PAHS - Emergency Department Protocol

Emergency
Patan Academy of Health Sciences

Department of General Practice and Emergency Medicine
November, 2015
Content
Title Page Number
Communicaiton skills 1-4
Clinical examinations 5-25
Emergency structure and operation 26-32
Resuscitation 33-67
Cardiac emergencies 68-79
Respiratory emergencies 80-97
Abdominal emergencies 98-119
Neurological emergencies 120-131
Metaboic emergencies 132-147
Toxicology 148-167
Common problems 168-180
Environmental injuries 181-184
Orthopedic injuries 185-192
Obstetrics and Gynecology emergencies 193-197
Psychiatry emergencies 198-199
Police cases 200-202
Procedures 203-221
Paediatric emergencies 222-284
If there are any corrections or updates in the protocol please send mail at ashisshrestha@pahs.edu.np
Communication Skills
Contents
Communication in crisis ..................................................................................................................................... 2
Crisis Resource management (CRM).............................................................................................................. 2
Three big CRM skills are ................................................................................................................................. 2
Close loop communication ........................................................................................................................ 2
Sharing information (SBAR) ....................................................................................................................... 2
Reassess ..................................................................................................................................................... 2
Delivering death notification ............................................................................................................................. 3
Griev_ing method .......................................................................................................................................... 3
What reaction to expect? .............................................................................................................................. 3
Medical Ethics .................................................................................................................................................... 4
PATAN ACADEMY OF HEALTH SCIENCES
Communication in crisis
“Communiation errors kill patients.”
Crisis Resource management (CRM)

Crisis Resource Management is the skill of managing the human and physical resources in a stressful, high-
stakes environment.
Three big CRM skills are

1. Uses closed-loop communication
2. Shares information
3. Reassesses
Close loop communication

“What is thought is not said, what is said is not heard, what is heard is not understood, what is understood
is not done, what is done is not confirmed.”
So close the loop by speaking up and confirming that the person you want to communicate has
understood.
Sharing information (SBAR)

• Situation
• Background
• Assessment
• Recommendation
Reassess
Ferquent reassessment is the key to success.
DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 2

Delivering death notification

Griev_ing method
Gather Collect family in quiet, respectful place
Resources Call for any additional support to assist the family with their grief
Identiry Identiry yourself, identify deceased patient by name, identify state of
knowledge of the family pertraining to the evens of the day. Are they aware
of possible death or will this be a completely unexpected event for them?
Educate Educate about event occurred in ED
Suggest to them that you are bringing a very bad news
Verify Verify that a family member had died
Space Give family member personal space and time for emotional moment
Inquire Ask them if they have any question
Nuts and bolts Allow relatives to see deceased
Take care of personal belongings
Give Give documents, express condolence
What reaction to expect?

Families may go into denial, anger or guilt. Family anger is not uncommon so prepare to react supportively.
Do not be defensive or judgemental if faced with statement of negligency or what should have been done.
Allow survivors to express their feelings. Remain clam and silent.

Medical Ethics
Medical ethics for practice:
Ethics is set of principles, values with the help of which we can arrive in right decision. Nothing in right or
wrong in ethics but it all depends on the situation. Something may be right for a person may not be right for
the other. There are few principles in ethics which we can utilize to get right decisions.
1. Autonomy: We should respect patients’ decision in every step. If the patient is incompetent or minor
(less than 16 years to give consent), we can seek help from surrogate decision makers.
2. Beneficence: Do good to the patient. Our every activity should be guided with this principle.
3. Non Maleficence: Do no harm to patient.
4. Justice: We should be guided with equitable distribution of resources.
Besides these principles, we can use some other theories like

• Consequentialism: If the result of the action is beneficial to the patient, we can do it.
• Utilitarian: The action should be guided with positive effect to everyone not only to the person.
• Deontology: every action should be guided by duty and if you are doing an action, you should think
that this action can be done to you or not.
• Confidentiality: we should maintain the confidentiality of the patients’ information as far as possible.
In case of written order from court of law, we can give information to the court only. Sometimes, to
protect society and other people, this principle is waived but we should inform patient before
breaching it.
• Medical Professionalism is a desire to help people and to help society as a whole with quality
healthcare. We should be guided by professionalism to provide good care to the patient.
• Informed Consent: There are three important component of informed consent.
o Information- we should provide adequate comprehensible information to the patient. We
should provide pros and cons of the procedure and consequences of not giving consent to
patient.
o Voluntariness – the consent should be given voluntarily without coercion.
o Competency: the person giving consent should be competent to give consent. They should
have good higher mental function without use of drugs that influence his competency.
In case of life saving and emergency procedure, we can take consent from the surrogate decision makers if
the patient is not competent.

Clinical Examination
Contents
General Examination.......................................................................................................................................... 5
Respiratory System ............................................................................................................................................ 8
Cardiovascular System ..................................................................................................................................... 13
Abdomen.......................................................................................................................................................... 18
Approach to Coma ........................................................................................................................................... 22
Neurological Examination ................................................................................................................................ 25
General Examination
Skin
• Generalized absence of skin pigmentation occurs in albinism. Syndrom with features of albinism are
– Chediak Higashi syndrome – Phagocytic deficiency disease, Phenylketonuria (Inborn error of
amino acid metabolism)
• Patchy absence of skin pigmentation may be due to vitiligo
• Circumscribed hypopigmentation of lesion of skin occurs in – Hansen’s disease, Tenia vesicolor
• Generalized hyperpigmentation – Hemochromatosis, Addison’s, Cushing’s
• Patchy hyperpigmentation – Pellagra, Scleroderma
• Yellow pigmentation of skin: Jaundice, Carotenemia, Long standing severe anemia
• Bluish discolourisation: Cyanosis; Ruddy complexion: Polycythemia; Pallor: Decrease in Hb
• Diabetes Mellitus
o Necrobiosis lipodica diabetocorum – Papulo nodular lesion enlarging to form brownish
yellow plaque with waxy surface over front of leg.
o Diabetic dermopathy – Dull, red, oval, flat topped
o Diabetic bulla – over legs, hands, feets bilaterally healing with atrophic scars
o Diabetic rubeosis – flushed skin of face
o Carotenoderma – yellowish tint of skin due to deposition of carotene
o Granuloma annulare – popular lesion over central area of body and flexures of neck, arm
and thing
o Sclerederma diabeticorum – diffuse waxy, non pitting, induration of skin particularly over
back of neck and upper trunk
o Infection like furuncle, carbuncle
• Chronic renal failure
o Uraemic frost
o Erythema papulatum uraemicum – erythematous nodules over palm, soles and forarm
o Generalised puritis
o Metastatic calcification
o Kyrle’s disease – multiple discrete or confluent hyeperleratotic follicular papules over lower
extrimities
o Nail change – proximal white and distal half pink
o Oral manifestations – coating of tongue, xerostomia, ulcerative stomatitis
• Internal malignancy
o Acanthosis nigricans – adenocarcinoma of GIT
o Plamo planter keratoderma – Ca bronchus and oesophagus
o Nectolytic migratory erythema – glucagonoma
o Pityriasis rotunda – hepatocellular Ca
o Sign of Leser Trelat – sudden eruption of intensely pruritic multiple seborrhoeic keratosis in
Ca stomach

o Migratory thrombophlebitis in Ca panceas

o Cutaneous hamartoma – Ca breast, thyroid, GI polyposis = cowdens disease
Face
Forehead
• Prominent forehead: Acromegaly, Chronic Hyerocephalus, Rickets, Thalassemia
• Wrinkling of forehead:
o Bilateral: Anxiety, Bilateral ptosis as in Myasthenia Gravis, Bilateral III nerve palsy, Bilateral
Horner’s syndrome
o Unilateral: Unilateral ptosis as in unilateral III nerve palsy, Horner’s syndrome
• Absence of wrinkling of forehead
o Unilateral: Bell’s palsy
o Bilateral: Myotonic dystrophy, hyperthyroidism (Joffroy’s sign)
Eyes
• Ptosis, Pallor, Icterus, Bitot’s spot (Vitamin A deficiency), Arcus senilis
Tongue
• Macroglossia: Acromegaly, Down’s syndrome. Tumors
• Microglossia: Pseudobulbar palsy, Facial hemiatrophy
• Fissured tongue: Down’s, Vitamin B deficiency, Acromegaly, Congenital malformation
• Hairy leukoplakia: EB virus, typically seen in lateral margin of tongue
Stature
• Stature is total height measured from vertex of head to sole of feet. Upper segment is vertex of
head to symphysis pubis. Lower segment is from symphasis pubis to sole of foot.
• Stature > Arm span: Adrenal cortex tumor, precocious puberty
• Arm span > stature: Hypogonadism, Marfan’s syndrome, Klinefelter’s syndrome
• Upper segment > lower segment: Adrenal cortex tumor, precocious puberty
• Lower segment > Upper segment: Hypogonadism, Marfan’s syndrome, Klinefelter’s syndrome
• Gigantism: Height more than six feet six inch. Dwarfism is height less than four feet.
Obesity
• Generalised obesity: Uniform distribution of fat throughout the body.
• Android obesity: Obesity characterized by excess deposition of fat over region of waist.
• Gynoid obesity: Characterised by excess deposition of fat over region of hip and thigh.
• Superior or central obesity: Excess fat deposition over face, neck and upper part of trunk –
cushing’s syndrome
Posture
• Parkinsonian posture: Universally flexed posture
• Cerebellar posture: Stands with feed wide apart and is unable to maintain a steady posture while
standing. Patient is ataxic on sittine (trunkal ataxia) when vermis of cerebellum is affected.

• Decrebrate posture: Extension of elbows and wrist with pronation of arm. Lesion is at brainstem
disconnecting the cerebral hemispheres from the brainstem.
• Decorticate posture: Flexion of elbows and wrist with supination of the arms. It suggest severe
bilateral hemispherical damage above the midbrain.
Nail
• Koilonychia – spoon shaped: Iron deficiency, IHD, Syphillis, Hemochromatosis
• Beau’s line – Transverse ridge in the nail plate due to temporary alteration of nail growth rate:
Acute febrile illness, Pneumonia, MI
• Plummer nail – Onycholysis of nail: Hypothyroidism, Raynaud’s disease
• Lindsay nail – Proximal dull white portion and a distal pink or brown with a well demarcated
transvere line: Uraemia
• White nail (Terry Nail) – White color in the nail bed than nailplate: Anaemia, CCR, DM, Malignancy
• Red nail: CCF, Blue nail: Wilson’s disease
• Black nail: Peutz Jeghers syndrome, Cushing’s syndrome, Addison’s disease
Fever
• Maximum normal oral temperature: 6 am – 98.6, at 6 pm – 99.6
• Normal diurnal variation is 1 degree F, rectal temperature is 1 degree F more than oral. Oral
temperature is 1 degree F more than axillary
Fever with relative bradycardia
• Typhoid Fever, Meningitis, Viral fever (Influenza), Brucellosis, Leptospirosis, Drug induced fever
Fever with exanthema

• Rash appearing on first day of fever – Chicken pox
• Rash appearing on fourth day of fever – Measles
• Rash appearing on seventh day of fever – Typhoid
Patterns of fever
• Continuous: The temperature remains elevated above normal without touching the baseline and
the fluctuation does not exceed 1 degree F. E.g. Lobar pneumonia, infective endocarditis, enteric
fever
• Remittent: Temperature fluctuation exceeds 1 degree F but without touching baseline: abscess
• Intermittent: Temperature touches the baseline in between. E.g. sepsis. Quotidian fever is a hectic
fever occurring daily
• Relapsing: Febrile episodes are separated by normal temperature for more than one day.
o Tertian fever: Occuring alternate days, Pl vivax, Pl falciparum, Pl ovale
o Quartan fever: Occuring every two ays, Pl malariae
o Pel Ebstein fever: Lasting 3-10 days followed by afebrile period of 3-10 days. Hodgkins
o Saddle back fever: Initially fever lasts 2-3 days followed by a remission lasting for 2 days and
then fever reappears and continues for 2-3 days. Dengue fever
o Cyclic neutropenia: Fever occurs every 21 days.

Respiratory System
General Examination
Built, Nourishment, Dyspnoea, Cyanosis
Clubbing
• Normal angle of nail and nail bed in 160 degree and is known as Lovibond angle.
• Grading of clubbing:
• Grade I: Obliteration of the angle between the nail and the nail bed and positive fluctuation test
• Grade II: Parrot beak appearance
• Grade III: Drumstick appearance
• Grade IV: Hypertrophic osteoarthopathy – Painful swelling of wrist, elbow, knee, ankle with
radiographic evidence of subperiosteal new bone formation.
• Scharmroth’s sign: When the dorsum of the distal phalanges of the fingers of both hands are
approximated to each other, a diamond shaped gap is made. This gap disappears with clubbing.
• Causes of clubbing
Pulmonary CVC GI Miscellaneous
o Bronchogenic carcinoma o Cyanotic o Cirrhosis of o Syphillis
o Metastatic lung disease congenital heart liver o Syringomyelia
o Suppurative lung disease disease o Ulcerative o Acromegaly
(Bronchiectasis, cystic fibrosis, o Bacterial colitis o Thyrotoxicosis
lung abscess, empyema) endocarditis o Chron’s
o ILD o Atrial myxoma disease
o Longstanding PTB o Eisenmenger’s o GIT malignancy
o Chronic bronchitis syndrome
o Mesothelipma
o Neurogenic diaphragmatic tumor
o Pulmonary AVM
Scaroidosis
Inspection
Inspection of upper respiratory tract
Oral cavity, nose, pharynx
Inspection of lower respiratory tract
Supraclavicular area, Infraclavicular area, Mammary region, Axillary region, Infra axillary region,
Suprascapular region, Interscapular region, Infrascapular region
Position of Trachea
Trial Sign: Prominence of clavicular head of sternocleidomastoid on the side to which trachea is
deviated.
Position of Apex beat
Symmetry of Chest
• Drooping of shoulder
• Hollowness or fullness in supraclavicular and infraclavicular fossa

• Crowding of ribs, Kyphosis or Scoliosis

Chest Deformities
• Flat Chest: Anterior posterior and transverse diameter ratio 1:2 (Normally 5:7) – TB, Fibrothorax
• Barrel Chest: Anterior posterior to transverse diameter 1:1 – COPD (Emphysema)
• Pigeon Chest: Forward protusion of sternum and subcoastal cartilage – Marfan’s syndrome,
Childhood asthma, Rickets
• Pectus Excavatum (Funnel chest, cobbler’s chest): Hollowness of lower end of sternum – Marfan’s
syndrome
• Harrison’s sulcus: Indrawing of ribs to form symmetrical horizontal grooves above the costal
margin, along the line of attachment of diaphragm due to hyperinflation of lungs and repeated
strong contraction of the diaphragm – Chronic respiratory disease on childhood, Childhood asthma,
Rickets, Blocked nasopharynx due to adenoid enlargement.
• Ricket rosary: Bead like enlargement of costochondral jounction – rickets
• Scorbutic rosary: Sharp angulation with or without beading or rosary formation of the ribs arising as
a result of backward displacement of pushing of sternum – Vitamin C deficiency
Overlying skin
• Engorged veins and subcutaneous nodules – Sarcoid and malignancy
• Intercostal scar – Drained pleural effusion, empyema or pheumothorax
• Discharging sinus – TB
• Empyma nessitans – Intercoastal swelling close to sternum
Chest movement
• Rate: Normal is 14-18 per minute. Tachypnoea is more than 20 per minute. Bradypnoea is decrease
in respiratory rate. Hyperponea is increase in depth of respiration (Acidosis, Brain stem lesion,
Anxiety).
Rhythm
Regular abnormal breathing patterns
• Chyne stokes breathing: Hyperpnoea followed by apnoea – Cardiac
failure, Renal failure, Narcotic drug poisoning and raised ICP
• Kassmaul’s breathing: Increased rate and depth of breathing –
Metabolic acidosis, pontine lesion.
Irregular Abnormal Breathing Pattern

• Biots breathing: Apnea between several shallow or few deep
inspiration – Meningitis
• Ataxic breathing: Irregular breathing where deep or shallow
breathing occurs randomly – Brainstem lesion
• Cogwheel breathing: Interrupted breathing seen in nervous individual.
• Pursed lip breathing: Breaths against pursed lip to increase endobronchial pressure above the
surrounding alveoli and prevents its collapse – COPD

Palpation
Trachea
• Position of trachea is confirmed by slightly flexing the neck so that chin remains in the midline. The
index finger is then inserted in the suprasternal notch and tracheal ring felt. Slight shift of trachea
to the right is normal.
Tracheal Tug – Olliver’s sign
• This sign is elicited by standing behind patient. The chin of the patient is raised and cricoid cartilage
is held up on deglutition on either side with finger of both hands. The sign is said to be positive
when downward tug is belt by the fingers during cardiac systole.
o Positive: Aortic arch Aneurysm
o False Positive: Mediastina tumor attached to aortic arch
o False negative: Non pulsatile aortic aneurysm (Thrombosed)
Inspiratory Tracheal descent

• Tracheal decent with inspiration – COPD
Confirmation of Apical impulse
Measurement of Chest Expansion
In male at the level of nipple, in female below breast. Measured with measuring tape. Normal expansion is
5-8 cm. In severe emphysema it is less than 1 cm. Non respiratory cause - Ankylosing spondylitis.
Assessing symmetry of chest expansion
• Upper thorax: Examiner facing patient’s back and placing hand over the patient’s supraclavicular
fossa. The extent of upward movement in quiet respiration is compared on both sides.
• Anterior thorax: Both hand placed by the side of rib cage with thumb towards midline. After a deep
breath, the degree of expansion is compared on both sides by movement of thumb away from the
midline.
• Posterior thorax: Similar posteriorly
Tenderness over chest wall

• Empyema; Local inflammation of parietal pleura, soft tissue and osteomyelitis; Infiltration with
tumor; Amoebic liver abscess
Detection of subcutaneous emphysema
• Injury to chest wall and rib, pneumothorax, rupture oesophagus
Others
• Vocal fremitus: Felt over chest wall on asking patient to speak (99-99 or 1-1-1). Increased in
consolidation, decreased in pleural effusion.
Percussion
Anterior chest wall
• Supraclavicular region (Kronig’s Isthmus): Band of resonance 5-7 cm above supraclavicular fossa.
Bounded medially by scalenus muscle, laterally by acromion process, anteriorly by clavical and

posteriorly by trapezius. Percussion is done by standing behind patient. Hyper resonance –

Emphysema; Impaired resonance – Pulmonary TB, Malignancy in apex
• Clavicle: Directly over medial 1/3rd of the clavicle
Lateral chest wall

• 4th to 7th intercostal spaces
Posterior chest wall

• Suprascapular – above spine of scapula
• Interscapular
• Infrascapular up to eleventh rib
Percussion on right side

• Liver dullness from right 5th ICS up to right costal margin
• Tidal percussion: To differentiate upward enlargement of liver or subdiaphragmatic abscess. If on
deep inspiration, the previous dull note in the fifth right intercostal space on the mid clavicular line
becomes resonant, it indicated dullness was due to liver, if persists it is due to lung pathology.
Percussion on left side
• Traub’s space:
o Surface anatomy:Two parallel vertical lines are drawn from 6th costochondral junction and
9th rib in mid axillary line. These two lines are connecte with a horizontal line from 6th ICS
above an costal margin below.
o Boundaries: Right side – Left lobe of liver, Left side –Spleen, Above – Left lung resonance,
Below – Left costal margin, Content – Fundus of stomach
o Traube’s space is obliterated in: Left pleural effusion, massive splenomegaly, enlarged left
lobe of liver, full stomach, fundal growth, and massive pericardial effusion.
o Traube’s space is shifted upward in: Left diaphragmatic paralysis, Left lower lobe collapse,
Fibrosis of left lung.
Others
• Percussion tenderness: Present in empyema and inflammation of parietal pleura.
• Straight line dullness: Present in hydropneumothorax
• Shifting dullness: Dull area percussed in axilla in sitting position becomes resonant in lying. Shifting
occurs immediately in hydropneumothorax and very slowly in pleural effusion.
• S shaped curve of ellis: In moderate pleural effusion, the uppermost level of dullness in highest in
the axilla and lowest in the spine and tend to assume the shape of S.
Auscultation
General principles
• Diaphragm is preferred.
• Patient should breath with mouth open to prevent sound being produced from a partially closed
nose.

• Avoid auscultation 2-3 cm from midline in the upper part of chest – bronchial breathing is normal
here
• Hairy chest should be moistened.
• Auscultation after coughing is a useful procedure. It helps differentiate coarse crepitation and low
pitched ronchi from pleural rub. Coughing does not alter pleural rub but alters ronchi and crackles.
Breath Sounds
• Vesicular breath sound: Low pitched, Inspiration longer than expiration (3:1), no pause in between.
Breath sound is decreased in: Asthma (Silent chest), Tumor, Pleural effusion, Pleural thickening,
Collapse lung with occluded bronchus, Emphysema.
• Bronchial breath sound: Loud, high pitched, prolong expiration with pause between inspiration and
expiration.
o Tubular: High pitched – Consolidation, Collapse, Above pleural effusion
o Cavernous: Low pitched – Thickened wall cavity with communicating bronchus
o Amphoric: Low pitched with high tone and a metallic quality – Smooth walled cavity,
Broncho-pleural fistula, tension pneumothorax
• Crackles: Nonmusical, interrupted added sounds of short duration. Fine Crackles: Less loud and
arise from Alveoli. Coarse Crackles: Low pitched and arise from bronchioles and bronchus.
o Early inspiratory – chronic bronchitis, Mid Inspiratory – Bronchiectasis, Late inspiratory –
Asbestosis, pulmonary fibrosis, pneumonitis, interstitial lung disease, pulmonary edema,
Expiratory - chronic bronchitis, pulmonary edema.
• Wheeze
o Fixed monophonic: Single note of constant pitch, timing and site. Results from air passage
through localized narrowing of airway. Seen in – Tumors, Foreign body, Bronchial stenosis,
Intrabronchial granuloma.
o Random polyphonic: Scattered in inspiration and expiration. E.g. Bronchial asthma
o Expiratory polyphonic: Complex musical sound continuing finally to end in expiration due to
expiratory compression of large central airways. E.g. Emphysema
o Sequential inspiratory wheeze: Opening of distal airway which has become abnormally
opposed during previous expiration. E.g. pulmonary fibrosis, fibrosing alveolitis, asbestosis.
• Sounds
o Bronchophony: Appears to be heard near earpiece – consolidation, cavity communicating
with bronchus, above level of pleural effusion
o Aegophony: Nasal or bleating quality. On saying E it will be heard as A – consolidation,
above level of pleural effusion.
o Whispering pectoriloquy: Whispering voice at the end of respiration is transmitted without
distortion – consolidation.
o Pleural rub: Superficial, localized grating sound best heard with firm pressure with
stethoscope and not altered by coughing, associated with pain.
o Pleuro – pericardial rub: Adjacent to pericardium being moved across on another by cardiac
pulsation.

Cardiovascular System
General Examination
Pulse
Rate, Rhythm, Volume, Description Example
Character Pulse
Hypokinetic pulse Small volume pulse with narrow Cardiac failure, Shock, MS, AS
pulse pressure
Hyperkinetic pulse Large volume and wide pulse High output – Anaemia, fever,
pressure beriberi; MR, VSD
Anacrotic pulse (Pravus et Low amplitude pulse with slow Severe AS
Tradus) rising and late peak
Pulsus Dicroticus Single pulse wave with one peak LVF, Dehydration, DCM, Cardiac
in systole and one peak in temponade
diastole
Pulsus Bisfreiens Single pulse wave with two peak AS, Severe AR, HOCM
Pulsus Bigeminus Normal beat followed by Digatilis toxicity
premature beat and
compensatory pause
Pulsus alternans Alternating large and small LVF
volume pulse
Pulsus paradox Fall in systolic BP more than Cardiac temponade, constrictive
10mm hg during inspiration pericarditis, airway obstruction,
SVC obstruction
Pulsus paradoxus: Inflate the BP cuff to suprasystolic level and deflate at the rate of 2 mmHg per beat, The
peak systolic pressure during expiration is noted. The cuff is then deflated even more slowly and the
pressure is again noted when Koratkoff sound becomes audible throughout the respiration
Blood Pressure
• Korotkoff sounds
• Phase 1: First appearance of clear, tapping sound. It represents the systolic BP
• Phase 2: Tapping wounds are replaced by murmur
• Phase 3: Murmurs become louder
• Phase 4: Muffling of sounds
• Phase 5: Disappearance of sounds
Jugular Venous Pressure

When measure with the patient reclining at 45 degree it is normally about 4-5 cm. Right atrial
pressure is 0-8mmHg and at SVC it is 1-6mmHg. The measured JVP can be converted to mmHg by
multiplying with 0.736. In JVP: a wave is due to atrial contraction, c wave is doe to closure of mitral
and tricuspid valve, x descent is due to atrial relaxation, v wave is due to venous filling right
ventricular contraction, y descent is due to atrial emptying.
Causes of elevated JVP

Unilateral non pulsatile Innominate vein thrombosis

Bilateral non pulsatile SVC obstruction, Massive right sided pleural
effusion
Bilateral pulsatile Cardiac: HF, TR, TS, Constrictive pericarditis,
Cardiac temponade
Pulmonary: COPD, Corpulmonale
Abdominal: Ascities, Pregnancy
Iatrogenic: Excessive iv fluid
Kussmaul’s sign: Inspiratory rise in JVP: Constrictive pericarditis, restrictive pericarditis, RV infract, RF
failure
Friederich’s sign: Rapid fall and rise of JVP: Constrictive pericarditis, TR
Abdominal jugular reflex: Pressing periumbilical area transiently raises JVP by 3 cm and falls down even
when pressure is continued, whereas in patents with right or left hart failure, the JVP remains elevated.
Systemic Examination
Inspection
Precordium bulge suggests LVH since child hood
Visible Pulsation
Carotid artery pulsation Hyperdynamic states, AR, Coarctation of aorta,
HTN
Aortic pulsation Dilation of ascending aorta, Aortic aneurysm, AR
Pulmonary artery pulsation Pulmonary artery dilatation, High output states,
Pulmonary HTN, Pulmonary hypercirculation
(ASD)
Suprasternal pulsation AR, Aortic arch aneurysm, Thyrotoxicisis,
Coarctation of aorta
Supraclavicular pulsation AR, Subclavian artery aneurysm
Sternoclavicular pulsation AR, Aortic dissection, Aortic aneurysm
Left parasternal pulsation RVH, MR
Apical pulsation LV or RV hypertrophy
Ectopic pulsation IHD, Left ventricular dysfunction, Aneurysm,
Cardiomyopathies
Inter and infra scapular pulsation Coarctation of aorta – Suzman’s sign
Epigastric pulsation Aortic aneurysm, RVH
Hepatic pulsation TS, TR
Chest wall defects: Pectus excavatum, Pectus carinatum

Costal cartilages: Costochondritis
Spine: Kyphosis, scoliosis, ankylosing spondylitis.
Palpation
Apical impulse: 1 cm medial to mid clavicular line or 10 cm lateral to midsternal line in 5th
intercoastal space. Normal displacement is 1 cm in lateral decubitus position. Normal apical impulse

is confined to one intercoastal space and has an area of 2.5cm square. Normal duration of thrust of
apical impulse is less than 1/3 of systole.
Abnormalities of apical impulse

Absent apical impulse Behind the rib or sternum, Dextrocardia
Tapping apical impulse Papable S1: Mitral stenosis
Hypodynamic apical impulse (felt with decrease Acute MI, Pleural effusion, Pericardial effusion,
thrust) Constrictive pericarditis, COPD
Hyperdynamic apical impulse: Increase in LV volume overload: AR, MR, VSD, PDA
amplitude without an increase in duration; >1/3 <
2/3 of systole and occupies more than one ICS
Heaving apical impulse: Increase both in amplitude LV pressure overload: AS, HTN, Coarctation of
and duration: >2/3 of systole and occupies one ICS aorta
Diffuse apical impulse Left ventricular aneyrysm
Double-Triple-Quadruple apical impulse HOCM
Parasternal Impulse
Anterior movement of left parasternal area as felt by palm of hand in right ventricular enlargement
and left atrial enlargement.
Shocks: Palpable heart sound

• Aortic area: A2 – Systemic HTN; Aortic ejection click – Congenital valvular aortic stenosis
• Pulmonary area: P2 – Pulmonary HTN: Pulmonary ejection click – Pulmonary valvular stenosis
• Apical: S1- MS; Opening snap- MS; S3-DCM; S4-HOCM
Thrills: Palpable murmur – base of fingers

Thrills Systole Diastole
Carotid AS
Aortic AS Acute severe AR, Syphilitic AR
Pulmonary PS, ASD, VSD PDA
Loft lower parasternal VSD
Apex MR, AS MS
Percussion
Useful only is detecting aortic dilatation as in Aortic aneurysm and pulmonary dilatation as in
pulmonary Hypertension
Auscultation
Mitral area – Apex; Tricuspid area – lower left sternal border; Aortic area – 2nd ICS left, pulmonary
area – 2nd ICS right; Erb’s area – second aortic area, 3rd left ICS, Gibson’s area – 1st ICS left, PDA is
best heard.
Auscultation areas: Carotids, Inter and infrascapular areas, Axilla, Supra and infraclavicular areas

Abnormalities of S1
Soft Loud Variable
MR, TR, RV or LV dysfunction, MS, TS, High output state, Short AF, Extrasystole, Complete
TS, MS(calcified valve), Obesity, PR heart block
AR-acute, Prolong PR interval
Splitting RBBB with pulmonary HTN, Left ventricular pacing, Ectopic beats
from LV
Reverse splitting Right ventricular pacing, Ectopic beat from RV
Abnormalities of S2
Absent Soft Loud
Old age due to A2: AS A2: Systemic hyperperfusion, Aortic aneyrysm, atherosclerosis
calcified AS, P2: PS P2: Pulmonary HTN, Pulmonary artery dilation
Emphysema
Splitting S2 Wide Early A2: MR, VSD, Constrictive pericarditis
variable Late P2:RBBB, Left ventricular ectpics, Left ventricular pacemaker
Wide fixed ASD, RVF, Massive PE
Reverse splitting Early P2: WPW
Delayed A2: Hypertrophic caridiomyopathy, LBBB, Right ventricular pacemaker
S3
Physiological Pathological
Children, Young adult, Athletes, Pregnancy High output states, ASD, VSD, PDA, AR, MR, TR
S4: Hypertrophic cardiomyopathy, HTM, CAD

Heart Murmurs
Murmurs should be described in following ways: Area, Systolic/Diastolic, Timing (ESM, PSM, MDM, EDM),
Intensity (grading), Pitch (low or high), best heard (bell or diaphragm – MDM is best heard will bel),
conduction, posture (MDM of MS in left lateral position, EDM of AR in sitting and leaning forward),
variation of murmur with dynamic auscultation.
Levine and Freeman’s grading of Murmurs
Systolic Diastolic
I: Very soft I: Very soft
II: Soft II: Soft
III: Moderate III: Loud
IV: Loud with thrill IV: Loud with thrill
V: Very loud with thrill (heard with stethoscope)
VI: Very loud with thrill (Heard even with stethoscope slightly away
from wall)
Systolic murmur
Early systolic Mid systolic Late systolic Pansystolic
VSD, Acute severe TR, AS, PS, HOCM MVP, TVP, Papillary MR, VSD, TR
Acute severe MR muscle dysfunction

Diastolic murmur
Early Mid Late
AR, PR MS, TS MS, TS, Complete heart block
Uncommon mid diastolic murmurs

Carey-coomb’s murmur: Rheumatic valvulitis
Austin flint murmur: Chronic AR
Ritan’s murmur: Complete heart block

Abdomen
General Examination
• Nutritional status, Anaemia, Finger Clubbing, Leukonychia (Hypoalbuminaemia), Koilonychia (Iron
deficiency).
• Lymphadenopathy: Virchow’s node – Left supraclavicular node palpable in GI malignancy and in
pelvic malignancy (Troisier’s sign)
• Scratch marks of puritus, Kayser Fleisher ring – wilson’s disease
• Tylosis of plam in carcinoma of oesophagus
• Signs of liver failure
o Alopecia
o Fetor hepaticus – Sweetish, slightly fecal smell due to methyl mercaptan derieved from
methionine in hepatocellular failure
o Jaundice, parotid swelling, gynaecomastia
o Spider naevi: Central arteriole with radiating vessels due to increase circulating estrogen –
seen in SVC territory in liver failure and pregnancy
o Palmar erythema, Dupuytren’s contracture, Asterexis, Xanthelasma.
Inspection
Shape
• Generalized: Fat, fluid, flatus, faeces or fetus
• Localized: Symmetric and centered around umbilicus – small bowel obstruction; Asymmetrical –
liver or spleen or ovary
• Scaphoid or shrunken: Advance starvation or malignancy
Umbilicus
• Normal: slightly retracted and inverted. Everted –Unblical hernia. Slit – Vertical in pelvic or ovarian
tumor – Horizontal in ascities.
Movements
• Rise in inspiration and fall in expiration. In peritonitis abdomen is still.
Visible pulsation
• Seen in aortic aneurysm in thin patient
Visible gastric peristalsis (VGP) or intestinal peristalsis (VIP)

• VGP: Wave progressing from left hypochondrium and epigastric towards right lumbar region –
Gastric outlet obstruction.
• VIP: Step ladder form of peristaltic wave in umbilical region – small bowel obstruction.
Skin
• Striae atrophica or gravidarum: White or pink linear marks seen by gross stretching
• Purple striae: Seen in cushing’s syndrome
• Prominent superficial vein:
o Caput medusa: Distended vein around umbilicus in portal hypertension

o SVC obstruction: Blood flow in vein is caudally above umbilicus.

o IVC obstruction: In the area below umbilicus if flow is away from umbilicus – Portal
hypertension, if it is towards umbilicus – IVC obstruction. Veins should be examined in
standing position.
• Linea nigra: Pigment below umbilicus seen after pregnancy
• Cullen’s sign: Bluish discoloration of periumbilical region in hemorrhagic pancreatitis
• Grey Turner’s sign: Bluish discoloration in flank in hemorrhagic pancreatitis.
Measurement
• Abdominal girth is measured at the level of umbilicus.
• Distance between lower end of xiphisternum to xymphysis pubis – usually umbilicus is in midway.
Umbilicus is displaced downwards in cirrhosis with ascities and upward in ovarian or pelvic tumors.
• Spinoumbilical line: Line between anterior superior iliac spine and umbilicus is equal on both sides.
Shift of umbilicus to one side indicates tumors originating from other side.
Palpation
• Superficial and deep palpation followed by palpation of organ.
Liver
• Hand flat on abdomen with fingers pointing upward, lateral to rectus and so that finger tips are
parallel to expected edge of liver. Movement inwards and upwards and keep steady when patient
takes deep breath through mouth. Wait for one full phase of respiration and continue workup
laterally.
• Second method: Right hand below and parallel to costal margin. Palpate liver border against radial
border of index finger.
• Findings on palpation
o Soft, smooth, tender liver: Congestive liver failure, Acute viral hepatitis
o Firm and regular: Obstructive jaundice, cirrhosis, chronic congestive cardiac failure
o Nodular: Advanced secondary carcinoma, Hepatoma
o Pulsatile: Systolic pulsation – TR; Diastolic pulsation – TS
Gall bladder
• Palpable over lateral edge of rectus abdominis near tip of 9th costal cartilage on right – Ca head of
pancreas, Mucocele, Ca GB.
• Murphy’s sign: GB palpated during deep inspiration, at the height of inspiration the breath is
arrested with gasp as the mass is felt – acute cholecystitis.
Spleen
• Spleen is palpable only when it is enlarged 2-3 times towards right iliac fossa.
• Palpate from right iliac fossa to left hypochondrium, wait for one full respiration.
• At the height of inspiration release the pressure on the examining hand so that the finger tip slips
over the lower pole of spleen, confirming its presence and surface characterstics.
• Move examining hand upward till rib margin if spleen is not palpable.

• If still not palpable, position the patient in the right lateral position with the left hip and knee flexed
then place other hand posteriorly to support the lower rib cage and repeat the examination.
• Alternatively examine the patient from left side curling the fingers of left hand beneath the costal
margin as patient breaths deeply.
• Middleton’s maneuver: Examiner stands on the left side of the patient facing the foot of the bed.
The hooked fingers of left hand are placed under the costal margin and with right hand pressure is
exerted over the poster lateral aspect of the lower thorax. The patient is then asked to take a deep
breath and spleen is felt at the end of deep inspiration.
Kidneys
• Use bimanual technique placing one hand posteriorly below rib cage and the other over upper
quadrant. Push two hands together firmly to feel lower pole as the patient breathes in deeply.
Difference between Left Kidney and Spleen

Features Left Kidney Spleen
Location Posterior L1 region Anterior 9-11th rib
Edge Round Sharp
Notch Absent Present
Insinuation of fingers between Fingers can be Fingers cannot be insinuated
costal margin and the organ insinuated
Band of colonic resonance Present Absent
Enlargement Towards lumbar region Towards right iliac fossa (Since left colic
flexure and phrenicocolic ligament
prevent the direct onward elargement)
Movement with respiration Restricted Moves freely on inspiration
Bimanual palpation Palpable Non palpable
Ballotability Ballotable Not ballotable
Loin fullness and dullness Present Absent
Urinary bladder
Palpated in suprapubic region
Examination of groin, para aortic nodes and vessels
• Examine groin for hernia
• Palpate aorta and common iliac vessels
• Para aortic nodes are palpable along umbilical region and epigastrium along the let border of aorta
when considerably enlarged.
Tenderness
• Rebound tenderness: Inflammation of peritoneum
• Shifting tenderness: Mesentric adenitis
• Referred or crossed tenderness: Pressure applied over descending colon causes pain over right iliac
fossa – Rovsing’s sign
Percussion

Liver
• In normal liver upper border is in 5th ICS.
• Normal dullness over upper part of liver is reduced in: Severe emphysema, Large right
pneumothorax, Gas or air in peritoneal cavity.
• Dull percussion below costal margin is in hepatomegaly.
• Liver span: Normally 12-15 cm extending from 5th rib (or below nipple) to palpable border or right
costal margin
Spleen
• Nixon’s method: The patient is placed on right side so the spleen lies above the colon and stomach.
Percussion begins at the lower level of pulmonary resonance in the posterior axillary line and
proceeds diagonally along the perpendicular line toward the lower mid anterior costal margin. The
upper border of dullness is normally 6-8 cm above the costal margin. Dullness greater than 8 cm in
an adult is presumed to indicate splenic enlargement.
• Castell’s method: With supine, percussion in the lowest intercostal space in the anterior axillary (8th
or 9th) produces a resonant note on full inspiration suggests splenomegaly.
Bladder
• Superior and lateral borders can be defined from the adjacent bowel.
Fluid in abdomen
• Shifting dullness: About 1000 ml of fluid should be present to elicit this sign
• Fluid thrill: This is felt when there is large amount of fluid – more than 2000 ml.
• Puddle’s sign: Can detect as little as 120 ml fluid. Patient is to lie in the prone position for 5 minutes
then goes to arm knee position. Percussion around umbilicus gives dull note
• USG can detect as little as 30 ml of fluid.
Auscultation
• Succssion splash: Pyloric stenosis, advance intestinal obstruction, Paralytic ileus, normal stomach
within 2 hours of meal.
• Bruit:
o AAA: Bruit can be heard left of the umbilicus
o Renal artery stenosis: Bruit over mid abdomen
o Bruit over common iliac artery can be heard in stenosis or aneurysm
o Bruit over liver may be heard in: Hemangioma, Hepatocellular carcinoma, acute alcoholic
hepatitis. Hepatic artery aneurysm
o Bruit can also be heard in coeliac artery stenosis and carcinoma of pancreas
Venous hum: It is heard between xiphisternum and umbilicus due to turbulence of blood flow in well-
developed collaterals as a result of portal hypertension (Cruveihier-Baugaren Syndrome). It signifies
congenital patent umbilical vein draining into portal vein.

Approach to Coma
State of Consciousness
Auditory, visual and noxious stimuli of progressively increasing intensity should be applied to the patient.
Respiration
Cheyne Stokes Breathing
• Rate of respiration will be around 30 per minutes.
• Waxing and waning respiration. Waning is followed by apnoea for about 15 seconds.
• Due to bilateral damage anywhere between forebrain and upper pons. Prolong circulation time due to
cardiac failure also produces Cheyne strokes breathing.
Central Neurogenic Hyperventilation

• Rapid breathing of 40-70 breaths per minutes. PaO2 > 70-80mmHg and PCO2 > 40mmHg
• Lesion of low midbrain ventral to aqueduct of Sylvius and upper pons ventral to fourth ventricle.
Apneustic Breathing
• Prolong inspiratory gasp with a pause at full inspiration.
• Lesion of dorsolateral lower half of pons.
Cluster Breathing
• Periodic respiration that are irregular in frequency and amplitude, with variable pauses between clusters
of breath.
Ataxic Breathing
• This is irregular rate and rhythm and is usually due to medullary lesions.
• Ataxic breathing and bilateral VI nerve lesions may be a warning sign of brainstem compression from an
expanding lesion in posterior fossa.
Pupil Size and Reactivity

Thalamic Lesion
• Small and reactive pupil. Also noted in many toxic metabolic conditions resulting in coma.
Hypothalamic Lesion
• Result’s in Horner’s syndrome (Ipsilateral Ptosis, Miosis, Anhidrosis and Exophthalmos)
• Lesion anywhere in sympathetic pathway causes Horner’s syndrome.
Midbrain Lesion
Dorsal Tectal Lesion
• Interrupt the pupillary light reflex, resulting in mid position eyes, which are fixed to light but react to near.
Ciliospinal reflex (Dilation of Ipsilateral pupil in response to pain applied to neck fact and upper trunk. Right
sided pupil size increases 1-2mm from baseline if right sided pain is applied) is preserved.
Nuclear Midbrain Lesion

• Affects both sympathetic and parasympathetic pathway resulting in fixed, irregular mid position pupils
which may be unequal.
Lesion of III nerve

• Lesion of III nerve in brain stem of after the nerve exits the brainstem cause wide pupillary dilation
unresponsive to light.
Pontine Lesion
• Interrupts sympathetic pathway to cause small pupils (pinpoint pupil) which remains reactive.
Lesion above Thalamus and below Pons

• Should leave pupillary function intact, except for Horner’s syndrome in medullary or cervical spinal cord
lesion.
Ocular Motility
Preservation of ocular motility implied that large portion of brainstem from oculomotor nucleus in midbrain
to the vestibular nuclei at the Ponto medullary junction in intact. Evaluation of ocular movement consists of
three main elements.
Abnormalities of resting position including eye deviation.
Spontaneous eye movement
• Purposeful appearing eye movements occur in locked in syndrome, catatonia, pseudo coma and persistent
vegetative state.
• Rowing eye movement indicates intact brainstem and coma due to metabolic or toxic cause or bilateral
lesion above brainstem.
• Nystagmus is due to irritative or epileptogenic supratentorial focus.
• Spontaneous conjugate vertical eye movements like ocular bobbing which is characterized by rapid
downward jerk of both eyes followed by a slow return to the mid position. The center of lesion is Pons
• Occulopalatal Nystagmus occurs to damage in lower brainstem involving Gullain Mollaret triangle, which
extends between the cerebellar dentate nucleus, red nucleus and inferior olive.
Reflex Ocular Movements

Oculocehpalic reflex (Doll’s eye movement)
• As head rotates to right eye moves to left if the test is positive.
Cold Caloric Testing

• Head is tilted back 60 degree from the horizontal plane.
• 10 ml of ice cold water is slowly injected into ear canal.
• There is a slow conjugate movement of eye towards stimulated ear which is corrected with Nystagmus fast
phase towards the opposite ears.
• Warm water irrigation produces reversal of flow. COWS (Cold water opposite, Warm water same side)
• Normal response indicate intact brainstem.
• Absent response indicate brainstem involvement.
• Abnormal dysconjugate response occur with cranial nerve palsies, internuclear ophthalmoplegia or
restrictive eye disease.

Motor System
Posture
• Head and eye deviation to one side and contralateral hemiparesis indicate supratentorial lesion, while
ipsilateral hemiparesis indicates brainstem lesion.
• Decerebrate posturing is bilateral extensor posture, with extension of lower extremities and adduction and
internal rotation of shoulders and extension at elbows and wrist. This is due to bilateral mid brain or pontine
lesion. Less commonly deep metabolic encephalopathy or bilateral supratentorial lesion involving the motor
pathways may produce similar pattern.
• Decorticate posturing is bilateral flexion at the elbows and wrists with shoulder adduction and extension
of the lower extremities. Usually lesion is above the brainstem.
• Unilateral dcerebrate or decorticate posture may be due to lesion anywhere in the motor system from
cortex to brainstem.
Adventitious Movements
• Tonic clonic or other stereotyped movement indicates seizure.
• Myoclonic jerking, nonrhythmic jerking movements in single or multiple muscle groups is seen with anoxic
encephalopathy or other metabolic comas such as hepatic encephalopathy.
• Rhythmic myoclonus which must be differentiated from epliptic movements is usually a sign of brain stem
injury.
• Tetany occurs with hypocalcaemia.
• Cerebellar fits, resulting from intermittent tonsillar herniation are characterized by a detoriation of level
of arousal, opisthotonos, respiratory rate slowing and irregularity and pupillary dilation

Neurological Examination
Examination of higher mental function
Consciousness
State of awareness of self or environment.
Confusion
Lack of clarity and coherence of thought, perception, understanding or action. First feature of cognitive
impairment.
Coma
State of unconsciousness in which patient does not respond to any external or internal stimuli.
Stupor or Semi-consciousness
State of disturbed consciousness from which only vigorous external stimuli can produce arousal.
Coma Vigil (Vegetative State)

Patient is comatose but eyelids are open giving appearance of being awake. Patient may perform random
limb and head movement but there is complete inability to respond to command or to communicate.
Akinetic mutism
Partial or fully awake patient who is immobile and silent. This state may be seen in hydrocephalus, mass in
region of third ventricle or large bilateral hemispherical lesion.
Abulia
Mild form of Akinetic mutism. Patient is hypokinetic but is able to communicate. This is seen in lesion in
the periaqueductal region, lower diencephalon.
Locked in Syndrome (Pseudo Coma)

Patient is awake and alert but non communicable with intact lid movement, eye movement in vertical
plane, quadriplegia and involvement of lower cranial nerve. The lesion is in ventral pons or bilateral
medulla with intact tegmentum (RAS).
Catatonia
Patient appears awake and blink spontaneously. There is waxy flexibility (Maintains the posture
implemented by examiner). This is seen in schizophrenia.
Delirium
Acute confusion state characterized by period of agitation, heightened mental activity, increase
wakefulness, hallucinations, motor hyperactivity and autonomic stimulation. There is impaired attention.
Dementia

It is a syndrome of acquired global or multifocal impairment of cognitive function involving decline in

intellect, memory or personality in the presence of normal consciousness.
Orientation
Time, Place, Person and Self
Handedness
Dominant side is tested by asking patient to kick ball or to use his eye to see through a small hole. On
asking patient to fold arm across chest, dominant hand is placed anteriorly. There is an anatomic difference
between the sizes of dominant and non-dominant cerebral hemisphere. Planum temporale which is
adjacent to the auditory center of Helschl’s transverse gyrus is larger in the left hemisphere in the right
handed individual.
General Intelligence
• Abstract thinking
o Patient is asked to explain the meaning of common proverb.
• Reasoning
o Patient is asked to compare object or asked to differentiate between lie and mistake.
• Judgment
o Asked questions like what would you do on seeing house on fire.
• Attention
o Asked to subtract 7 from 100 down to zero.
• Calculation
o Patient is asked to solve simple numerical problem.
• Memory
o It is a power to retain and recall past experiences.
Components of Memory
• Reception
• Registration
• Retention
• Recall
Types of Memory
Immediate or short term memory
• It is a memory for event of few seconds duration.
• Patient is asked to spell “World” backward.
• Impaired in acute confusion syndrome, Wernicke-Korsakoff syndrome.
• Recent memory
• Recall of information presented within minutes, hours or days.
• Patient is asked to remember three unrelated common objects told to him few minutes ago.
• Long term or secondary or remote memory
• Memory for past events.
• Tested by asking dates of some of public events

Perception
Delusion
These are false beliefs which continue to be held despite evidence to the contrary.
Hallucination
These are false impressions referred to the organs of special senses in the absence of a stimulus.
Illusion
These are misinterpretations of stimuli.
Obsession
These are recurrent and persistent thoughts which intrudes into the patient’s mind despite best effort to
get rid of them.
Visuospatial Function
Ask the patient to copy a drawing of five pointed star or three dimensional box. Constructional apraxia or
visuospatial agnosia results in difficulty in drawing the lines.
Apraxia
It is a defect in the ability to carry out known acts in the absence of motor weakness, sensory loss or ataxia.
Agnosia
Failure to recognize known objects in the presence of intact sensory, visual and auditory pathway.
Sleep
Non REM has four stages and lasts about 90 minutes and progressed to REM sleep. Most of the dreaming
occurs in this stage.
Speech and Language

Aphasia
• Broca’s aphasia or expressive aphasia or motor aphasia
• Poorly articulated and non-fluent speech with reduced number of words with errors of grammar
and syntax. Wernicke’s aphasia or receptive aphasia or sensory aphasia
• Speech is fluent but may contain jargon.
• Conduction aphasia
• Patient is unable to repeat words or phrase spoken by examiner. The lesion is in perisylvian area
with damage to the fibers or arcuate fasciculus.
• Transcortical aphasia
• Broca’s or Wernicke’s type aphasia with normal repetition.
• Global aphasia
• Broca’s and Wernicke’s type aphasia
Dysarthria
• Cerebellar Dysarthria
• Patient speaks slowly and deliberately, syllable by syllable.

• Pseudo-bulbar (spastic) Dysarthria

• Individual syllabus are slurred and the precision of consonant pronunciation is lost.
• Bulbar Dysarthria
• Nonspecific slurring of speech. Dysphagia and nasal regurgitation are present.
• Rigid Dysarthria
• Low volume monotonous speech. Extrapyramidal involvement – Parkinsonism.
• Cortical Dysarthria
• Irregular hesitancy in word production associated with difficulties I abstract, volitional movements
of lips and tongue.
Examination of Cranial Nerves

Olfactory - I
The only sensory nerve with no thalamic connection.
• Loss of smell – Anosmia
o Nasal disease, Head injury, Tumors or anterior cranial fossa, Chronic basal meningitis.
Kallman’s syndrome, Tabes dorsalis, Internal hydrocephalus, Aging, Alzheimer’s disease,
Parkinson’s, Huntington’s chorea, Down’s syndrome.
• Increase olfactory acquity – Hypersomia
o Migraine, Addison’s, Hyperemesis gravidarum, Strychnine poisoning
• Perversion of smell – Parosmia
o Severe nasal infection, Phenytoin, Psychological
• Foul smell – Cacosmia
o Upper respiratory tract infection or atrophic rhinitis
• Olfactory hallucinations
o Epilepsy arising from uncinated gyrus of temporal lobe, psychosis.
Optic nerve – II
• Visual Acuity
o Snellen’s chart is used.
o Pin hole test: If the patient is able to see through pin hole then patient has refractive error.
• Visual Field
o Normally visual field is 1000 temporally, 600 nasally, 600 superiorly and 750 inferiorly.
• Color Vision
o Ishihara Chart
• Pupillary Reflex
o Bright light is swung from one eye to the other alternatively. The eye with optic nerve lesion
will show a positive consensual light reflex but will not show positive direct light reflex.
o Affected pupil starts to dilate when direct light is thrown into that eye – Marcus Gunn’s
Pupil
• Fundus
o Early papilloedema
 Blurring of superior and inferior margin of disc
 Disc hyperaemia and dilated capillaries
 Spontaneous venous pulsation are absent

 Splinter hemorrhages at or just off the disc margin

 Optic cup is preserved
o Established papilloedema
 Disc margin becomes indistinct and central cup is obliterated.
 Disc surface is elevated above the retina.
 Venous engorgement and peripapillary oedema
 Flame shaped hemorrhages and cotton wool spots.
 Radiating folds around macula
o Chronic paiilloedema
 Central cup remains obliterated.
 Hemorrhage and exudates gradually resolve.
o Atrophic papilloedema
 Retinal vessels are attenuated with perivascular sheathing.
 Dirty white appearance of optic disc due to reactive gliosis.
Oculomotor – III, Trochlear – IV and Abducent – VI

Ptosis
• Partial
o Occurs with lesion of the cervical sympathetic pathway (Horner’s syndrome) due to
weakness of tarsal muscle innervated by cervical sympathetic nerves. The upper eyelids can
however be raised voluntarily.
• Complete
o The patient is not able to voluntarily open the affected eye. This is due to paralysis of levator
palpabrae superioris innervated by III.
Size of Pupils
• Normal size of pupil is 3-5mm. Pupil less than 3 mm is called mitotic and > 5mm is called mydriatic.
Pin point pupil is said to be present when pupillary size is less than or equal to 1 mm.
• Miosis
o Old age, Horner’s syndrome, Drugs or toxins (Neostigmine, Morphine, OP poisioning),
Pontine hemorrhage.
• Mydriasis
o Infancy, Lesion of III (Midbrain), Drugs (Atropine, Pethedine), Optic atrophy.
Pupillary reflexes
• Light reflex
o Light reflex is carried by optic tracts to Edinger Westphal nucleus bilaterally and then
through ciliary ganglion to sphincter pupillae by the ciliary nerves.
• Direct light reflex
o Patient is asked to look at a distance to avoid accommodation reflex. When light is projected
into eyes the pupil constricts.
• Consensual reflex
o Reflex is elecitated by placing partition between two eyes. When light is projected into one
eye other eye respond by constricting.
• Reaction to accommodation

o Afferent stimulus goes to optic nerve then to occipital lobe, fibers pass to the frontal lobe
and from here corticobulbar fibers go to third nerve nucleus.
o The reflex comprises of adduction (convergence) of eyes and pupillary constriction when
patient looks at near object.
• Agryl Robertson pupil is absent accommodation reflex and preserved light reflex – Syphilis, DM,
Alcoholic polyneuropathy.
Ocular Movements
Tested by holding object 60 cm away from eye of the patient.
• Diplopia
o Two types of diplopia. Uniocular and binocular. In binocular diplopia there is always true
and false image formation. True image is near to eye and clear while false image is farther
from eye and unclear. Red glass test is done to detect affected eye in patient with diplopia.
A red glass is placed in front of affected eye visualizes false image as red.
• Squint
o Abnormality of ocular movement in which visual axis do not meet at the point of fixation.
• Upper motor Neuron (Supranuclear) Lesion
o Lesion of supranucleus causes conjugate gaze paralysis.
• Lesion of PPRF – Lateral conjugate gaze paralysis
• Lesion of midbrain at the level of superior colliculus – Upward gaze paralysis
• Lesion of midbrain at the level of inferior colliculus – Downward gaze paralysis
• Fronto-mesencephalic pontine pathway
o Contraleteral Brodmann’s area -> Corona radiate -> Internal capsule -> Cerebral peduncle ->
Decussates at the level of pons -> Descends to synapse contralateral pontine paramedian
reticular formation (PPRF).
• Parital and temporo mesencephalic pontine pathway
o Paritral lobe -> Temporal lobe -> Pons -> Medial longitudinal fasiculus about the level of VI
nucleus.
• Internuclear lesion
o Lesion is in medial longitudinal fasiculus.
o Characterised by failure of adduction of eye on the side of leion of MLF and mild weakness
of abduction with Nystagmus on the contralateral side.
• Nystagmus
o Pendular Nystagmus
o Rapid horizontal oscillations to either side of the midline of equal amplitude seen on
forward gaze. Causes: Visual defect in infancy, chorioretinitis.
o Jerky Nystagmus
o Ocular oscillation of unequal amplitude with slow drift in one direction and fast correcting
movement in the other direction. Fast phase determining the direction of Nystagmus.
Horizontal Nystagmus is due to lesion of vestibular nerve, medial longitudinal bundle or
cerebellum. Vertical Nystagmus is due to condition involving brainstem. Rotatory
Nystagmus is seen in labyrinthine disorder.
 Grade I: Fast phase to left looking towards left only.
 Grade II: Fast phase to left looking straight ahead.

 Grade III: Fast phase to left looking towards right.
Trigeminal Nerve – V
Sensory system
• Pain, temperature and light touch are examined
• Opthalmic division
o Upper part of the side of nose
• Maxillary division
o Malar region and lip.
• Mandibular division
o Chin and anterior part of tongue.
Motor system
• Masseter and Temporal Muscle are palpated while patient clenches his jaws.
• Lateral Pterygoids weakness causes jaw to deviate paralyzed side on opening mouth.
Reflexes
• Corneal reflex
o Afferent is trigeminal nerve and efferent is facial nerve. Eyelid blinks when cornea is
touched.
• Jaw jerk
o Patient is asked to open mouth slightly. The forefinger placed below lower lip is tapped with
percussion hammer. There is slightly palpable upward jerk. It is exaggerated in
pseudobulbar palsy.
• Glabellar reflex
o Afferent is trigeminal nerve and afferent is facial nerve. Percussion of supraorbital ridge
results in bilateral contraction of the orbicularis oculi muscle.
Facial Nerve – VII

Motor
• All facial muscles are innervated. Upper part of the face has bilateral innervation while lower part
has unilateral innervation. So in UMN lesion upper part of face of affected side is spared.
Sensory
• Anterior two third portion of each half of the tongue is examined.
• Saliva is wiped after protruding tongue. Tongue must be protruded during entire test.
• Sugar, salt, citric acid and quinine is tested for sweet, salty, sour and bitter.
• Patient is asked to identify pointing the specific taste written in the card.
Secretory function
• Lacrimation
o Schirmer’s test: Blotting paper is placed under the lower eyelid and removed after 5 minutes.
Normally at least 10 mm of the blotting paper will be dampened by the evoked tear secretion.
• Nasolacrimal reflex

o Reflex secretion of tears by stimulation of nasal mucosa by irritating substance such as dilute
solution of ammonia or formaldehyde. Afferent is trigeminal nerve and efferent is greater superficial
petrosal nerve which is a branch of facial nerve.
• Salivation
o Highly flavored substance is placed in tongue and patient is asked to elevate copious, a copious
supply of saliva is seen to flow from the submandibular duct.
• Reflexes
o Corneal reflex
o Stapedial reflex
• Afferent is vestibulochochlear nerve and efferent is facial nerve. When the stapes is stimulated by loud
noise, noamally the reflex contraction of stapedius leads to reduction in transmission of the sound. Patient
may complain of hyperacusis for low tones.
Vestibulocochlear Nerve – VIII

Auditory function by use of the human voice
• Normal conversation voice should be heard at 20 feet and whispering voice should be heard at 10
feet.
• Non test ear should be occluded. Examiner should use unfamiliar words.
Watch test
• Quartz watch should be avoided.
Tunning fork test

A 512 Hz tuning fork is used.
Rinne’s Test
• Air conduction more than bone conduction = Positive
• Positive: Normal ear, Sensorineural deafness
• Negative: Conductive deafness
Weber’s test
• No lateralization – Normal ears
• Lateralization to normal ear – Sensorineural deafness on opposite side
• Lateralization to affected ear – Conductive deafness on the same side
Absolute bond conduction test (Schwabach test)

• Examiner should have normal auditory function.
• Bone conduction of examiner is compared with patients.
• ABC equal – Normal
• ABC increased for patient – Conductive deafness
• ABC decreased for patient – Sensorineuronal deafness
Audiometric test
• Test of vestibular function
Fistula sign
• Increasing pressure over external acoustic meatus by otoscope or repeatedly pressing tragus of the
ear against auditory meatus proguces nystamus.

Oculocephalic reflex (Doll’s eye movement)

• Normal response for the patient’s eye to deviate to the left as the head is turned to the right. It is a
definite sign of normal midbrain function. Its absence suggests brain death.
Positional vertigo
• Vertigo is induced by certain head postures or by sudden change in the head position.
Caloric test
• Head is elevated to 30 degree to bring semicircular canal into the vertical plane.
• Patient is instructed to fix upon a point in central gaze.
• External ear canal is irrigated with water at 300 C and then 440 C for 30-40 seconds each.
• COWS: Nystygmus -> Cold water Opposite side, Warm water Same side -> Normal response
Glosopharyngeal – IX and Vagus – X

• General sensation and taste over posterior 1/3 of tongue.
• Palatal reflex: Elevation of soft palate on saying ah.
• Gag reflex: Contraction of pharynx in stimulating pharynx.
Accessory Nerve – XI
• Testing of sternocleidomastoid muscle by turning face against resistance.
• Trapezius muscle testing by shrugging shoulder.
Hypoglossal Nerve – XII

• Patient is asked to move tongue.
Spinomotor System
Nutrition (Bulk of muscle)
• Muscle wasting is a sign of lower motor neuron lesion.
• Both sides should be compared.
o Circumference of limbs is measured at the following levels o Upper limb: 10 cm above and
below olecranon
o Lower limb: 18 cm above superior border of patella and 10 cm below tibial tuberosity.
Tone
Degree of tension of muscle at rest. Tone can be assessed by inspection, palpation of muscle group and
passive movement of joint. In unconscious patient raising an arm in turn and allowing it to fall back.
• Hypertonia
o There is a resistance felt on the passive movements of the joints either in form of spasticity
or rigidity.
• Spasticity
o Hypertonia of either agonist of antagonist group of muscle. Hypertonia of antigravity muscle
group produces clasp knife rigidity. In hemiplegia tone of flexor group of muscle exceeds
extensor.

• Rigidity
o Hypertonia is in both agonist and antagonist group of muscle.
• Plastic of lead pipe rigidity
o Uniform resistance offered to passive movement. E.g. Parkinsonism, Basal ganglia
neoplasm.
• Cog Wheel Rigidity
o Resistance offered to passive movement interrupted by alternate contractions of agonist
and antagonist muscle due to presence of associated tremor. E.g. Parkinsonism, CO
poisioning
• Hypotonia
o On inspection the muscle group is lax and assume a pendulous shape, on palpation the
muscle group is flabby to feel and there is diminished resistance to passive movement of
joints.
• Clonus
o Sudden stretching of hypertonic muscle produces reflex contraction. Ankle clonus is
demonstrated by dorsiflexing the foot after the hip. Patellar clonus by sharply moving
patella downward. Sustained clonus is a sign of pyramidal tract lesion.
• Myotonia
o This is a state in which muscle contraction continues beyond the period of time. When the
patient is asked to smile and then relax his facial muscle, a delay in relaxation of the muscle
is noted and the smile remains fixed on the face for longer.
• Power
o Grade 5 – Normal power
o Grade 4 - Movement against resistance
o Grade 3 – Movement against gravity
o Grade 2 – Gravity eliminated movement
o Grade 1 – Flicker of contraction
o Grade 0 – No movement
Coordination
• Finger nose test
o Patient is asked to keep limb outstretched and touch tip of his nose with forefinger.
• Finger-finger nose test
o Patient is asked to touch examiner’s tip of forefinger and then his own nose.
• Tapping a circle test
o A circle 1 cm diameter is drawn and patient is given a pencil and asked to tap out a series of
dots all within the circle.
• Dysdiadochokinesis
o Failure to efficiently perform rapidly alternating movements.
• The heel knee test
o Patient is asked to place heel of one foot over the knee of the other foot and then to move
the heel down over tibia.
• Foot pat test

o The patient is asked to pat the ground with the heels of the both feet alternatively in the
siting position.
Involuntary movements
• Chorea
o Semi purposive, irregular, non-repetitive and brief jerky movements. Due to involvement of
Caudate Nucleus.
• Athetosis
o This is a slow writing movement, best seen at wrist, fingers and ankles. The fingers writhe,
the wrists flex the forearm and arm rotate inwards, adduct and then rotate outwards in
abduction. The foot is inverted. The movements are absent during sleep, minimally altered
by eye closure, increased by voluntary movement and interfering with it. Due to
involvement of Putamen.
• Hemiballismus
o Involve proximal joint of one arm resulting in wild, rapid, flinging movement of wide radius
occurring constantly, interspersed with short periods of freedom. Due to involvement of
Subthalamic Nucleus.
• Dystonias
o Involuntary sustained muscle contraction. Due to involvement of Putamen.
• Tremors
o Rest tremors
 Tremor occurs when limb is at rest. Parkinson’s disease, Extrapyramidal disease
o Postural tremors
 Tremor occurs when limb maintains a posture like holding the arms and hands
outstretche. Thyrotoxicosis, Anxiety, Alcohol, Caffeine, Structural brain disease
o Intentional tremor
 Tremor occurs when the limb approaches its target. Lesion of cerebellum and its
connections: Multiple sclerosis, vascular disease.
Abnormalities of gait
• Circumduction gait
o In patient with hemiplegia.
• Spastic gait
o Bipyramidal lesion involving both the lower limb.
• High stepping gait
o Seen in patient with foot drop.
• High stepping and stamping gait
o Seen in patient with posterior column lesion. There is high stepping with forceful landing of
the foot.
• Ataxic gait
o Seen in cerebellar lesion
• Shuffling gait
o Seen in patient with lesions in extrapyramidial system. Patient makes a series of small, flat
footed shuffles.

• Waddling gait
o Seen in patient with proximal muscle weakness. Patient walks on broad base with an
exaggerated lumbar lordosis.
Reflexes
The components of reflex arc are; sensory receptor, afferent pathway, centre, efferent pathway, efferent
organ. Deep tendon reflexes are monosynaptic reflexes and the superficial and visceral reflexes are
polysynaptic reflexes.
• Abdominal reflexes
o Reflexes are retained till late in motor neuron disease and lost early in multiple sclerosis. In
hemiplegia there is unilateral loss of abdominal reflex.
• Plantar reflex
o Classical method: Stroking lateral aspect of sole of foot.
o Gorden reflex: Calf muscle are squeezed
o Oppenheim reflex: Firm stroke with the finger and thumb is applied don either side of the
anterior border of tibia, greater pressure being applied to the medial side.
o Chaddock reflex: Stroke is applied down the lateral malleolus.
o Minimal pyramidal lesion: Applying stimulus on the dorsolateral aspect of foot.
o Medial stimulation: Assessing the density of lesion.
o Extensor plantar response
 This response is seen in lesion of corticospinal tract. There is dorsiflexion of great toe
with extension and fanning of other toes.
 Equivocal
• Planter response is said to be equivocal in following situations
o There is a rapid but brief extension of toes at first which is followed by
flexion or predominant flexion followed by extension.
o There is only extension of great toe or extension of great toe with
flexion of small toes.
o There is no response to planter stimulation particularly if there is
paralysis of dorsiflexors.
o There may be flexion of knee and hip with no movements of toes.
 Minimal plantar response
• On eliciting the plantar reflex, no movement of the toes may be seen. The
presence of positive plantar response can then be assessed by feeling for the
contraction of tensor fascia lata and adductors of thigh.
o Pseudo Babinski sign
 False Babinski sign may occur in absence of pyramidal tract lesion in following
conditions.
 Sensitive individual
 As a response of plantar hyperesthesia.
 In athetosis or chorea where big toe may extend as a response of dystonic posturing.
 If short flexors of toes are paralysed due to LMN lesion.
 Infancy
 Deep sleep

 Deep anaesthesia
 Narcotic overdose
 Alcohol intoxication
 Coma secondary to metabolic disturbances
 Post traumatic states
 Post ictal states
 Cheyne stokes respiration
Differentiation between Babinski Pseudo Babinski

Babinski and Pseudo Babinski
Sign Traits
Hamstring contraction Felt Not felt
Pressure on the base of great Does not inhibit the extensor Inhibits extensor plantar
toe while eliciting the plantar plantar response response
reflex

Emergency Structure and Operation
Contents
Emergency Infrastructure ................................................................................................................................ 26
Resuscitation Bay and Team Dynamics ........................................................................................................... 27
Resuscitation Team ...................................................................................................................................... 28
Close loop communicaitons ......................................................................................................................... 28
Triage ............................................................................................................................................................... 29
Occupational Exposure and Universal Precaution........................................................................................... 30
Hepatitis B Exposure .................................................................................................................................... 30
HIV Exposure ................................................................................................................................................ 30
Universal precaution .................................................................................................................................... 31
Tetanus Prophylaxis ......................................................................................................................................... 32
Emergency Infrastructure

Resuscitation Bay and Team Dynamics

Resuscitation Team
Close loop communicaitons

Triage
Patient arriving at
Airway Assessment Ye No further

Signs of airway obstruction assessment,
• Cannot speak handover the patient
• Stridor or gurgling sound immediately to
RED
No
Breathing Ye No further
Respiratory rate > 30 assessment,
handover the patient
immediately to
No RED
Circulation Ye No further
SBP < 90 mmHg assessment, RED
CRT > 2 sec handover the patient
immediately to
RED
Mental Status
Cannot follow simple command Ye Handover the
patient immediately
No
CAN PATIENT WALK (Provided there is no
injury to limb)?
OR Transfer to
No
No potential life threatening condition Yellow
• Penetrating Injury Yellow
• High velocity collision
Ye
Transfer to
Green
Classification of Triage Category according to Symptoms
RED YELLOW GREEN
Unconscious Stable vitals with Stable vitals with
Ongoing seizure • Abdominal injury • Walking wounded
Sudden onset retrosternal chest • Fall from height • Weakness of limbs
pain • In moderate to severe • Fever
Respiratory Distress pain • Cough
Actively Bleeding • Palpitation

Occupational Exposure and Universal Precaution
Hepatitis B Exposure
Vaccination and Source is HBsAg positive Source is HBsAg Source is unknown or

antibody status of negative not available for
exposed workers testing
Unvaccinated/Nonimm HBIG and HB vaccine HB vaccine HB vaccine

une
Previously vaccinated
Non responder No treatment No treatment No treatment
Known non responder HBIG and Re - No treatment If known high risk

Vaccination source treat as HBsAg
positive
Antibody response Test for antibody No treatment Test for antibody

unknown If inadequate HBIG and If inadequate HBIG
HB vaccine and HB vaccine
If adequate - no If adequate - no
treatment treatment
HIV Exposure
Recommendation for HIV PEP for percutaneous injuries
Exposure HIV positive - HIV positive - Known source but Unknown source HIV Negative
type Asymptomatic Symptomatic HIV status cannot
be determined
Less 2 Drug PEP 3 Drug PEP No drug but No drug but No PEP
severe consider 2 drug consider 2 drug
PEP for source PEP for source
with risk factor with risk factor
More 3 drugy PEP 3 drugy PEP No drug but No drug but No PEP
Severe consider 2 drug consider 2 drug

Recommendation for HIV PEP for mucous membrane and non intact skin exposure
Exposure HIV positive - HIV positive - Known source but Unknown source HIV Negative
type Asymptomatic Symptomatic HIV status cannot
be determined
Less 2 Drug PEP 2 Drug PEP No drug but No drug but No PEP
severe consider 2 drug consider 2 drug
More 2 drugy PEP 3 drugy PEP No drug but No drug but No PEP
Severe consider 2 drug consider 2 drug
Basic Two Drug Regimen

Zidovudine 300 mg BD or 200 mg TDS + Lamivudin 150 mg BD
Expanded Three Drug Regimen

Basic Two drug regimen plus Lopinavir/Ritonavir combination 400/100 mg BD
Universal precaution
• Hand washing
• Gloves
• Mask and shields
• Gowns
• Disposals
• Environmental and work practice condition

Tetanus Prophylaxis
1. A clean wound
a. If previously receceived vaccine within 10 years
i. Vaccine not needed
b. If not received vaccine within 10 years
i. Vaccine needed
c. If vaccine status unknown
i. Vaccine needed
2. Contaminated wound
a. Primary tetanus prophylaxis not known – needs TIG
b. Primary tetanus prophylaxis more than 5 years – Vaccine needed
c. Primary tetanus prophylaxis less than 5 years – Vaccine not needed

Resuscitation
Contents
Adult Basic Life Support ................................................................................................................................... 34
Pediatric Basic Life Support ............................................................................................................................. 35
Advance Cardiac Life Support (Pulse less VT/VF) ............................................................................................ 36
Advance Cardiac Life Support (Asystole/PEA) ................................................................................................. 37
Pediatric Advance Life Support ........................................................................................................................ 38
Primary Trauma Care ....................................................................................................................................... 39
2015 ACLS Updates .......................................................................................................................................... 42
Anaphylaxis ...................................................................................................................................................... 44
Sign and symptoms ...................................................................................................................................... 44
Pathophysiology of Anaphylaxis .................................................................................................................. 44
Treatment of Anaphylaxis ............................................................................................................................ 45
Disposition of Patients with Anaphylaxis..................................................................................................... 46
Acid Base Disorder ........................................................................................................................................... 47
Basic Interpretation ..................................................................................................................................... 47
Advance Interpretation................................................................................................................................ 47
Primary pH Changes and Compensation ................................................................................................. 47
Acute Respiratory Acidosis (acute hypoventilation)................................................................................ 47
Chronic Respiratory Acidosis (ie. chronic hypoventilation) ..................................................................... 47
Acute Respiratory Alkalosis (ie. acute hyperventilation)......................................................................... 48
Chronic Respiratory Alkalosis (chronic hyperventilation) ....................................................................... 48
Metabolic Acidosis (ie. acute and chronic) .............................................................................................. 49
Metabolic Alkalosis (ie. acute and chronic) ............................................................................................. 50
Approach to Acid-Base Disorders ............................................................................................................ 52
Sepsis................................................................................................................................................................ 55
Definitions .................................................................................................................................................... 55
3 hour Bundle............................................................................................................................................... 55
6 hour Bundle............................................................................................................................................... 55
Documentation ............................................................................................................................................ 55
Antiboitics ........................................................................................................................................................ 56
Renal Dosing ................................................................................................................................................ 56
Bactericidal vs. Bacteriostatic antibiotics .................................................................................................... 56
Penicillins ..................................................................................................................................................... 56
Cephalosporins ............................................................................................................................................ 58
Aminoglycosides .......................................................................................................................................... 59
Fluoroquinolones ......................................................................................................................................... 60
Tetracyclines ................................................................................................................................................ 62
Sulfa drugs.................................................................................................................................................... 62
Nitrofurantoin .............................................................................................................................................. 63
Carbapenems ............................................................................................................................................... 63
Vancomycin .................................................................................................................................................. 64
Linezolid ....................................................................................................................................................... 64
Inotropes .......................................................................................................................................................... 65
Definitions .................................................................................................................................................... 65
Adrenergic Receptors .................................................................................................................................. 65
Commonly-Used Inotropes .......................................................................................................................... 65
Details .......................................................................................................................................................... 66

Adult Basic Life Support
Check for danger
Check responsiveness
Shout for help
Open airway
Not breathing normally?
30 chest compression
2 rescue breath
30 compressions
Attach to AED as
soon as available
Continue CPR
until qualified
personnel arrives
or signs of life
returns

Pediatric Basic Life Support
Stimulate and check responsiveness
Open Airway
Head tilt chin lift (jaw thrust)
Check Breathing If breathing

Look, Listen and Feel Recovery position
Yes
Breathe If no chest rise

Deliver 2 effective breaths Reposition airway
Reattempt breaths
Assess for the sign of circulation If no success

(Movement ± pulse) Treat as for airway
Do not delay > 10 seconds obstruction
No
Chest compression
30 compression 2 ventilation
Rate of about 100 compressions/minute
Continue
Resuscitation

Advance Cardiac Life Support (Pulse less VT/VF)
First Impression: Sick or

not sick? Assess ECG rhythm. Shockable? (Pulseless VT/VF)
Primary survey
Unresponsive Yes
Open airway, give 2 No
breaths
Give oxygen when
available
If no pulse, 30
compression 2 breath Shock (Defibrillation) x 1
Attach to Resume CPR 5 cycles (about 2 minutes)
AED/Monitor/Defibrilato without interrupting. Defibrillation
r
During CPR give vasopressor • Monophasic: 360J all shocks
Epinephrine 1mg every 3-5minutes • AED: Per manufacturer
Or • Biphasic: Per manual
Vassopresin 40IU in place of first or second • Biphasic unknown: 200J
Epinephrine initially, then same or
higher as first shock
Asystole No Assess ECG rhythm Reversible cause

PEA Shockable? • Identify and treat causes
o Hypoxemia
Yes o Hypovolemia
o Hypothermia
Shock (Defibrillation) x 1 o Hyeper/Hypokalaemi
Resume CPR 5 cycles (about 2 minutes) a and metabolic
Reassess/Monitor
without interrupting. disorders
• Airway
During CPR give consider antiarrythmic o Tamponade
• Oxygenation/ventilation
Amidarone 300mg IV/IO consider o Tension
• Paddle/Pad Position/
Contact repeat dose of 150mg x 1 in 5 minutes pneumothorax
• Effectiveness of CPR or o Toxins/poisons/drugs
• No Oxygen flow over Lidocaine 1-1.5mg/kg IV/Io initial dose o Thromboembolism
patient during shock (if Amidarone is not available)
Attempt/verify Then0.5-0.75mg/kg PRN every 5-10 min
• Advance airway position Maximum cumulative dose 3mg/kg
• Vascular access Consider Magnesium 2gm IV/IO
Monitor and treat for torsades de pointes
• Glucose Consider reversal cause of arrest
• Electrolyte
• Temperature

Advance Cardiac Life Support (Asystole/PEA)
First Impression: Sick or

not sick? Assess ECG rhythm. Shockable?
Primary survey
Unresponsive No Defibrillation
Open airway, give 2 Yes • Monophasic: 360J all shocks
breaths • AED: Per manufacturer
Give oxygen when • Biphasic: Per manual
available Resume CPR 5 cycles (about 2 minutes)
without interrupting. • Biphasic unknown: 200J
If no pulse, 30
initially, then same or
compression 2 breath During CPR give vasopressor
higher as first shock
Attach to AED/Monitor/ Epinephrine 1mg every 3-5minutes
Defibrillator
Reversible cause
Or
• Identify and treat causes
o Hypoxemia
Vassopresin 40IU in place of first or second
o Hypovolemia
Epinephrine
o Hypothermia
o Hyeper/Hypokalaemi
a and metabolic
disorders
Treat as pulse less Yes Assess ECG rhythm o Tamponade
VT/VF Shockable? o Tension
pneumothorax
Reassess/Monitor No
o Toxins/poisons/drugs
• Airway
Resume CPR o Thromboembolism
• Oxygenation/ventilation
• Paddle/Pad Position/ 5 cycles (about 2 minutes)
Contact
• Effectiveness of CPR
• No Oxygen flow over
patient during shock
Attempt/verify
• Advance airway position
• Vascular access
Monitor and treat
• Glucose
• Electrolyte
• Temperature

Pediatric Advance Life Support

BLS Algorithm: Assess and support ABCs as
needed
Provide oxygen
Attach monitor/defibrillator
Assess rhythm (ECG)

Shockable Not Shockable
VT/VF Asystole/PEA
Give 1 shock Resume CPR immediately

• Manual: 2 J/Kg Give Epinephrine
• AED > 1 year of age IV/IO 0.01mg/kg
Use pediatric system if available (1:10 000: 0.1ml/kg)
for 1-8 years Resume CPR Endotracheal tube: 0.1mg/kg
immediately (1:10 00: 0.1ml/kg)
Repeat every 3-5 minutes
Give 5 cycle of CPR
Give 5 cycle of CPR
Check rhythm No
Shockable rhythm? Is asystole go to box no 3 Check rhythm
If electrical activity No
Shockable rhythm?
Shockable
Check pulse Shockable
Continue CPR while defibrillator
is charging If no pulse go to
Go to VT/VF
Give 1 shock Asystole/PEA
• Manual: 2 J/Kg
• AED > 1 year of age If pulse present begin post
immediately resuscitation care
Give Epinephrine
IV/IO 0.01mg/kg
(1:10 000: 0.1ml/kg) Box 1
Tracheal tube: 0.1mg/kg • Push hard and fast (100/min)
(1:10 00: 0.1ml/kg)
• Ensure full chest recoil
Repeat every 3-5 minutes
• Minimize interruption in chest compression
• One cycle of CPR: 15 compressions then 2 breaths
Give 5 cycle of CPR
• 5 cycle = 1 to 2 minutes
• Avoid hyperventilation
Check rhythm No
• Secure airway and confirm placement
Shockable rhythm?
• After an advance airway is placed rescuers no longer delivers cycles
Shockable of CPR. Give continuous chest compression without pause for
breaths. Give 8 to 10 breathes per minute.
Continue CPR while defibrillator is charging • Check rhythm every 2 minutes
Give 1 shock • Rotate compression every 2 minutes with rhythm check
• Manual: 2 J/Kg • Identify and treat causes
• AED > 1 year of age o Hypoxemia, Hypovolemia
Resume CPR immediately o Hypothermia
Consider Antiarrhythmic o Hyeper/Hypokalaemia and metabolic disorders
Amidarone: 5mg/kg bolus IV/IO or lidocaine: o Tamponade
1mg/kg bolus IV/IO/TT or Magnesium 25 to 50
o Tension pneumothorax
mg/kg IV/IO for torsades de pointes of
o Toxins/poisons/drugs
hypomagnesemia (maximum 2g)
o Thromboembolism
After 5 cycle of CPR go to box 1

Primary Trauma Care

The following patient should go full trauma assessment
History:
• Fall >3 meters
• Motor vehicles accident with net speed > 30km/hr
• Thrown from vehicle/trapped in vehicle
• Death of a person in accident
• Pedestrian vs. car/cyclist vs car/unrestrained occupant
Examination
• Airway or respiratory distress
• BP>100mmHg
• GCs<13/15
• >1 area injured
• Penetrating injury
The assessment of trauma patient includes
1. Primary survey
A: Airway
B: Breathing
C: Circulation
D: Disability
E: Exposure
2. Secondary survey
Head examination
• Scalp and ocular abnormalities
• External ear and tympanic membrane
• Periorbital soft tissue injuries
Neck examination
• Penetrating wounds
• Subcutaneous emphysema
• Tracheal deviation
• Neck vein appearance
Neurological examination
• Glasgow coma scale
• Spinal cord motor activity
• Sensation and reflex

Chest examination
• Clavicles and all ribs
• Breathe sounds and heart tones
• ECG monitoring (if needed)
Abdominal examination
• Penetrating wound of abdomen requiring surgical exploration
• Blunt trauma – a nasogastric tube is inserted (not in the presence of facial trauma)
• Rectal examination
• Insert urinary catheter
Pelvis and limbs

• Fractures
• Peripheral pulses
• Cuts, bruises and other minor injuries
X rays (if possible)

• Chest x ray
• Cervical spine lateral view
• Pelvis and long bone x ray

Trauma patient
C spine protection
Airway assessment
Talk to patient
Signs of airway obstruction may include
• Snoring or gurgling
• Stridor or abnormal breath sounds
• Agitation
• Using accessory muscle of ventilation/Paradoxical chest movements
• Cyanosis
Airway not clear

Oxygen/Chin lift/Jaw thrust Airway clear
Reassess Suction
Guedel airway/nasopharyngeal airway
Intubation (if needed)
Breathing assessment
Look: cyanosis, chest movement, penetrating injury, use of accessory muscle
Feel: Tracheal shift, broken ribs, subcutaneous emphysema, percussion
Listen: Pneumothorax, detection of abnormal sounds in the chest
Breathing not clear

Oxygen
Reassess
Decompression and drainage of tension
pneumothorax
Closure of open chest injury
Artificial ventilation Breathing clear
Circulation assessment
Shock: Hypotension, tachycardia,
tachypnoea, pallor, cool extremities,
decreased capillary refill
Circulation not clear

Stop haermorrhage
Establish IV line with 2 large bore canula
Circulation clear
Administer IV fluid
Disability
A: Awake, V: Verbal response, P: Painful response, U: Unresponsiveness
Exposure
Secondary survey

2015 ACLS Updates

• If available, ECMO/ECPR should be considered for selected reversible causes of CA
• No vasopressin- no benefit and difficult to use
• Early epinephrine recommended
• Use of ultrasound to confirm ROSC and confirm ETT placement
• Use max 02 during CPR and titrate down after ROSC
• Low EtCo2 after 20 mins efforts = low likelihood of survival
• No routine lidocaine after ROSC (but may continue if started for VF/VT)
• PCI if: stemi, hemo/elec unstable if lesion suspected
• Post-arrest temp targeted to 32-36 with emphasis on avoiding fever
• Emphasis on CCR (cardiocerebral resus) vs CPR - uninterrupted compressions
• Emphasis on CAB vs ABC in ACLS - chest RECOIL is most important for improving flow/perf
• Delay airway for improved survival! (CAB) EXCEPT IN PEDS
• Although 30:2 comp:breath interval remains, Seattle hosp survival is highest in world and EHS uses
uninterrupted CPR with breaths Q10 compressions spaced btw
• AVOID PULSE CHECKS! - use etco2 as a measure of ROSC!!!
• ONLY STOP CPR TO SHOCK (even then, shocking with gloves has been ok’d)
SPECIFIC ISSUES:
Role of capnography: MANDATED.

• Goal 12-15 during CPR (below 10= suboptimal)
• Rise to 35-40 may indicate ROSC
• DO NOT TERMINATE until 35-40 maintained (not just spike)
Role of mechanical compression devices (autopulse or LUCAS)

• So far no hard evidence of survival/neuro benefit
• But this maybe due to a) comparison to very HQ CPR, b) unfamiliarity=lag to impliment’n
Role of antiarrhythmics in CA
• No med has shown long term survival benefit in CA
• Amiodarone has shown improved ROSC but overall equal death to lidocaine
• Ongoing trial comparing amio vs lido vs placebo - ALPS trial, out 2016
Role of dual shock therapy (?!)

• 1989 study shows no benefit but recent jobs case series showed benefit
• Expert recommendation to try if refractory VF an no other options
Role of vasopressors in CA
• No vasopressor has ever shown LT survival benefit in CA
• Epinephrine improves rates of ROSC
• Factors that may improve survival in subgroups:
o Early Epinephrine (first minutes)
o Consider avoiding in VF (likely due to MI - more vasoconstric)
o Definite use in PEA
o Not using too much… maybe titrate to etco2 drop (tho no evidence)

NOvel approach to assessmt of PEA: see Littman paper (2014) - SEE BELOW
• Ensure NOT TO INTERRUPT QUALITY CPR for US
When to call your code off?

• If unwitnessed, initial rhythm unshockable, and no prehosp ROSC - rare survival
• EtCO2 <10 after 20 mins HQ CPR and normothermic - consider termination
• Initial/recurrent Vfib - consider cath ASAP (mechanical cpr if available)
Post-arrest management (after ROSC)

o Start pressors early - MAP goal 65 (bp likely will drop when epi wears off
 Start peripherally if no central line available
o Place art line ASAP when possible (but don’t compromise HQ CPR)
o Cath lab?? - STEMI/VF/persistant HD compromise/high trop (SEE BELOW)
o Targeted temp management: 32-36 for those with persistent coma
 Relative contraind: ICH, hemorrhage, pregnancy
LITTMAN ALGORITHM (Littman et al. 2014)
WHO COULD BENEFIT FROM

CATH POST-ARREST:

Anaphylaxis
In general, anaphylaxis is underrecognized and undertreated. The triggers of anaphylaxis are not identified
in 66% of cases (even after rigorous investigation), but common precipitants include:
a. Foods (33% of cases) -- Most commonly nuts and shellfish
b. Medications -- Most commonly penicillins and cephalosporins
c. IV contrast dye
d. Blood products
e. Bites and stings
Sign and symptoms

1. Skin symptoms (90% of cases)
a. Can include hives, itching, flushing, swollen lips/tongue/uvula, periorbital edema, or
conjunctival swelling
2. Respiratory symptoms (70% of episodes)
a. Can include nasal discharge/congestion, change in voice, sensation of throat closure, stridor,
shortness of breath, wheeze, or cough
3. GI symptoms (up to 45% of episodes)
a. Can include nausea, vomiting, diarrhea, crampy abdominal pain
4. Cardiovascular symptoms (up to 45% of episodes)
a. Can include syncope, incontinence, dizziness, tachycardia, or hypotension
5. Biphasic anaphylaxis is defined as a recurrence of symptoms following resolution of the initial
episode (despite no additional exposure to the trigger).
a. Biphasic reactions have been reported in up to:
i. 25% of anaphylactic episodes in adults
ii. 10% of anaphylactic episodes in children
b. However, this frequency has likely decreased with the use of steroids.
6. The second reaction typically occurs within 8-10 hours of resolution of the initial symptoms--but
recurrences have been reported up to 72 hours later.
7. Death from anaphylaxis usually results from:
a. Asphyxiation due to upper airway edema
b. Respiratory failure due to bronchial obstruction
c. Cardiovascular collapse (less common)
Pathophysiology of Anaphylaxis
The original Coombs and Gell system classifies allergic reactions as Types 1-4:
• Type 1 (immediate hypersensitivity) -- IgE mediated
o Anaphylaxis is the most severe form of immediate hypersensitivity
• Type 2 (cytotoxic) -- IgG or IgM +/- complement mediated
• Type 3 (immune-complex) -- IgG or IgM +/- complement mediated
• Type 4 (delayed hypersensitivity) -- T-cell mediated
Irrespective of the mechanism, the acute management is identical.
Several mediators are released in anaphylactic and anaphylactoid reactions (eg. histamine, prostaglandins,
kinins, etc.) These mediators act on a variety of tissues: Vascular, Bronchial, GI

Histamine overview
Histamine binds to three types of receptors:
• H1-receptor -- Stimulation causes bronchoconstriction, increased vascular permeability, and
coronary artery spasm
• H2-receptor -- Stimulation causes increased inotropy, chronotropy, and gastric acid secretion
• H3-receptor (in the CNS) -- Stimulation mediates the synthesis and release of histamine
• H1-receptor blockers include: Diphenhydramine ("Benadryl"), -Cetirizine ("Reactine")
• H2-receptor blockers include: -Ranitidine ("Zantac"), -Famotidine ("Pepcid")
• Note that antihistamines work by blocking the histamine-receptor, not by degrading histamine
itself.
• Despite their common use in this setting, the evidence for H1-antihistamines in anaphylaxis is weak.
• H1-antihistamines may help to relieve itch and hives, but do not relieve airway obstruction or
hypotension
• There is no evidence for using H2-antihistamines in anaphyaxis. They are not included in most
modern guidelines
Treatment of Anaphylaxis
Resusucitation
• Fluids if hypotensive
• Consider early intubation if upper airway swelling
• Consider activated charcoal for recently ingested allergens (eg. peanuts)
IM Epinephrine
1. Epinephrine is the single most important medicine to give in acute anaphylaxis.
a. Even if given mistakenly (ie. to a patient who does not have anaphylaxis), the side-effects of
an IM dose of epinephrine are minimal (eg. self-limited tachycardia)
b. In contrast, failure to give Epinephrine in anaphylaxis is a risk-factor for death
c. As such, have a low threshold for giving IM epinephrine if anaphylaxis is suspected
2. Use the 1:1000 Epi concentration for IM dosing.
a. The dose is 0.01mg/kg (in peds) or 0.3-0.5mg (in adults) IM q5mins prn
b. With 1:1000 Epi, 0.5mg = 0.5mL
c. Inject IM (not SC) into the anterolateral thigh
d. Patients requiring >3-4 doses of IM Epi should be considered for IV Epi
Steroids
1. Solumedrol 40-125mg (1mg/kg in peds) IV
2. HC 500mg (5mg/kg in peds) IV
3. Either of these can be followed by Prednisone 50mg (1mg/kg) PO qd x 3 days.
+/- H1-antihistamines
1. The evidence for this is not strong, but it is a reasonable option
2. Diphenhydramine 50mg (1mg/kg in peds) IV

+/- Glucagon
1. This can be considered for patients on beta-blockers (who may be resistant to Epinephrine), or for
patients who are refractory to the treatments above
2. Glucagon works independently of beta receptors--and has inotropic, chronotropic, and smooth-
muscle relaxing effects
3. An initial dose of 1-5mg in adults (20-30ug/kg--to a maximum of 1mg in children) over 1-5 minutes
is recommended.
4. This can be repeated and/or followed by an infusion of 5-10mg/hour (in adults)
+/- Mg (only if asthma-related)

1. MgSO4 2-4g (50mg/kg) IV over 20 mins
IV Epinephrine
1) Use the 1:10,000 concentration for IV dosing.
2) The dose is 0.01mg/kg (in peds) or 0.1mg (in adults) IV given over 10 mins.
a) With 1:10,000 Epi, 0.1mg = 1mL
3) The adult dose (ie. 1mL) can be prepared as follows:
a) Draw up 1mL of 1:10,000 Epi (ie. the Epi in the crash cart)
b) Dilute this with 9mL of NS (to a total volume of 10mL)
c) Inject this 10mL volume over 10mins
Disposition of Patients with Anaphylaxis
1) Patients with mild-to-moderate symptoms who respond completely to treatment can be discharged
home after 2-6 hours of observation.
a) It is reasonable to give them a 3-day course of Prednisone to take home
2) Patients with severe attacks that respond promptly to treatment may warrant observation for up to 24
hours.
3) Practically-speaking, however, these patients may be candidates for discharge home after 6-12 housr if
they:
a. Did not have a life-threatening presentation
b. Responded completely to treatment
c. Are young and healthy
d. Live close to the hospital
e. Are being discharged home with family
4) Patients with life-threatening attacks warrant admission until at least 24 hours after full recovery.

Acid Base Disorder

Normal Values
• pH = 7.40
• PCO2 = 40 mmHg
• HCO3 = 24mmol/
• Anion gap
o If using Na - Cl - HC03, the normal AG is 12mmol/L.
o If using Na + K - Cl - HC03, the normal value AG is 16mmol/L
Basic Interpretation
Disorder pH PCO2 HCO3

Metabolic Acidosis  N or  
Metabolic Alkalosis  N or  
Respiratory Acidosis   N or 
Respiratory Alkalosis   N or 
Advance Interpretation
Primary pH Changes and Compensation
Overview
• Compensation is almost never "complete." That is to say, it almost never corrects the pH back to
7.40.
• "Overcompensation" essentially does not occur.
o The only exception is transient overcompensation that can occur during rapid shifts in pH,
PCO2, and HCO3.
o these rapid shifts can be quite common in sick patients--which can make ABGs in the
Emergency and ICU somewhat confusing
Acute Respiratory Acidosis (acute hypoventilation)
Etiologies of acute respiratory acidosis include:
• Acute CNS depression (eg. opioids, BZPs)
• Acute respiratory failure (eg. COPD, muscular weakness, GBS, myasthenia, botulism)
• Acute airway obstruction
During acute hypercarbia, every increase of 10mmHg in the PCO2 causes a drop of 0.08 in the pH.
• However, this pH change is only temporary--until renal compensation starts
Renal compensation for acute respiratory acidosis is as follows:
• Every increase of 10mmHg in the PCO2 causes an increase of 1mmol/L in the HCO3.
• This usually starts in 6-12 hours.
Chronic Respiratory Acidosis (ie. chronic hypoventilation)

Etiologies of chronic respiratory acidosis include:

• Chronic respiratory failure (eg. COPD)

• Obesity hypoventilation syndrome
Renal compensation for chronic respiratory acidosis is as follows:
• Every increase of 10mmHg in the PCO2 causes an increase of 4mmol/L in the HCO3.
• This is usually maximal within several days.
• The maximal HCO3 is ~45mmol/L.
o Additional CO2 retention after this point causes serum acidosis
Acute Respiratory Alkalosis (ie. acute hyperventilation)

Some etiologies of acute respiratory alkalosis include:
• Fear, anxiety, pain
• ASA toxicity
• Sepsis
• Large PE
• Stimulants
• Drug withdrawal
Acute respiratory alkalosis is much more common than chronic respiratory alkalosis--since most
precipitants of hyperventilation are either:
• Short-lived (eg. anxiety, fear, pain)
• Rapidly-fatal unless fixed (eg. ASA toxicity, sepsis, large PE)
During acute hypocarbia, every drop of 10mmHg in the PCO2 causes increase of 0.08 in the pH. However,
this pH change is only temporary--until renal compensation starts
Renal compensation for acute respiratory alkalosis is as follows:
• Every drop of 10mmHg in the PCO2 causes a drop of 2mmol/L in the HCO3
• This usually starts in 36-48 hours.
Chronic Respiratory Alkalosis (chronic hyperventilation)

Etiologies of chronic respiratory alkalosis include:
• CNS pathology (eg. brain tumor)
• Chronic liver disease
• Hyperthyroidism
• Pregnancy
Renal compensation for respiratory alkalosis is as follows:
• Every drop of 10mmHg in the PCO2 causes a drop of 2-5mmol/L in the HCO3.
• This is usually maximal by two weeks.
• The minimum HCO3 in this setting is ~12mmol/L.
• Chronic respiratory alkalosis is the only acid-base abnormality where the body can potentially
approach full compensation (ie. get close to 7.40).

Metabolic Acidosis (ie. acute and chronic)

Overview
• Respiratory compensation for metabolic acidosis begins immediately--and is maximal by 12-24
hours.
• The minimum PCO2 in this setting is ~5mmHg (in extremely ill patients)
• "Winter’s Rule" is used for primary metabolic acidosis.
o Winter's Rule calculates the expected PCO2 for a primary metabolic acidosis.
- Expected PCO2 = 1.5(HCO3) + 8 (+/-2)
o Winter's Rule works for both primary AG and non-AG metabolic acidosis.
• It does not work for metabolic alkalosis
Increased anion gap metabolic acidosis

• An increased anion gap suggests the presence of an acid that is either:
o Not normally present in the body (eg. formic acid in methanol overdose)
o Normally present in the body in only small quantities--but now present in large quantities
(eg. lactic acidosis)
• Specific etiologies of increased-AG metabolic acidosis include "MUDPILES CT":
o Methanol (ie. formic acid)
o Uremia (ie. phosphoric acid, sulfuric acid, ammonium)
o DKA, alcoholic ketoacidosis, starvation ketoacidosis (ie. ketoacids)
o Paraldehyde (ie. acetic and chloracetic acid)
• This is an older medication that was previously used for sedation and seizure control
o Phenformin/Metfomin (ie. lactic acid)
• Phenformin was an older biguanide that has since been replaced by Metformin
• Both agents can cause lactic acidosis in patients with renal failure
o Iron overdose, INH overdose (ie. lactic acid)
o Lactate (ie. lactic acid)
o Ethylene glycol (ie. glycolic and oxalic acids)
o Salicylates (ie. salicylclic, lactic, and ketoacids)
o Cyanide, carbon monxoide (ie. lactic acid)
o Toluene--from glue or solvent-sniffing
• An increased AG essentially always indicates the presence of a metabolic acidosis (irrespective of
any other acid-base disorders that may be present).
Low/normal anion gap metabolic acidosis

• This is caused by an imbalance of H+ and HCO3- in the body.
• Specifically, it can be caused by:
o Increased retention of H+
o Increased excretion of HCO3-
• Specific etiologies of a low/normal AG metabolic acidosis include "H-USEDCARP":
o Hyperalimentation
o Ureterosigmoid conduit
o Small bowel fistula

o Extra chloride (ie. hyperchloremia)

o Diarrhea
o Cabonic anhydrase inhibitors (eg. acetazolamide)
o Adrenal insufficiency
o Renal tubular acidosis (all types)
o Pancreatic fistula
• What these etiologies all have in common is that they cause either H+ retention or HCO3 excretion.
• In the Emerg and ICU, the most common cause of a low/normal AG metabolic acidosis is
hyperchloremic acidosis.
o This is usually caused by aggressive resuscitation with normal saline.
o It is characterized on bloodwork by:
- Decreased HCO3
- Normal or elevated Cl-
- Variable Na+
o The exact mechanism is controversial.
Co-existing metabolic acidosis and alkalosis

• An "increased-AG metabolic acidosis" and a "metabolic alkalosis" can co-exist.
o An anion gap is caused by acids which are not normally present.
• These acids are not eliminated by an increased HCO3
• For example, a patient with sepsis and vomiting can have an increased-AG metabolic acidosis (from
lactic acid), while simultaneously having a metabolic alkalosis (because of HCl loss from vomiting)
• In contrast, a "non-AG-metabolic acidosis" (caused by relative loss of HCO3) usually cannot co-exist
with a metabolic alkalosis (caused by relative retention of HCO3).
• One cancels out the other
The Delta Gap
• The Delta Gap is a corollary of the following two principles:
o With an isolated "elevated-AG metabolic acidosis", the rise in AG is approximately the same
as the fall in HCO3.
o With an isolated "non-AG metabolic acidosis", the rise in Cl is approximately the same as the
fall in HCO3.
• The Delta Gap = (AG - 12mmol/L) - (24mmol/L - HCO3)
o A normal delta gap is -6mmol/L to 6mmol/L
o A delta gap >6 suggests a metabolic alkalosis
o A delta gap <-6 suggests a non-AG metabolic acidosis
Metabolic Alkalosis (ie. acute and chronic)

Overview
• There are five main causes of metabolic alkalosis:
o Loss of H+
o Shift of H+ intracellularly
o Retention of HCO3

o Exogenous HCO3 (or equivalent).

• "Bicarbonate equivalents" are molecules that are metabolized to bicarbonate in the body
• They three main ones are lactate, citrate, and acetate
o Contraction alkalosis
• This is caused by loss of volume in the setting of a fixed quantity of bicarbonate
• It is generally poorly understood by most clinicians
• As mentioned, "Winter’s Rule" (for metabolic acidosis) does not work for metabolic alkalosis.
o Instead, use one of the following formulas to calculate "expected PCO2" in primary
metabolic alkalosis:
• Marino ("The ICU book," 3rd edition, 2006):
o Expected PCO2 = 0.7(HCO3) + 21 (+/- 2)
• Rosens, 7th edition:
o Expected PCO2 = 0.9(HCO3) + 9 (+/- 2)
o Unfortunately, these two formulas often give different answers (and it is unclear which is
the most accurate).
• The most common causes of metabolic alkalosis in hospital inpatients (ie. >95% of cases) are:
o Diuretics
o Vomiting
Classification of metabolic alkalosis
• Metabolic alkalosis can be classified as either:
o Chloride-responsive (more common)
o Chloride-resistant (less common)
Chloride-responsive metabolic alkalosis
• This is caused by either:
o Gaining HCO3 (or a HCO3 equivalent).
• -If HCO3- is gained, Cl- must be excreted to keep the body electrically neutral
o Losing chloride.
• -If Cl- is lost, HCO3- must be retained to keep the body electrically neutral
• Patients with a chloride-responsive metabolic alkalosis usually have a:
o Low serum Cl
o Low urinary Cl (ie. <10-15mmol/L)
• Specific etiologies of chloride-responsive metabolic alkalosis include:
o Upper GI loss of chloride
• Vomiting
• NG suction
o Long-standing diuretic use
• This promote loss of chloride
o Milk-alkali syndrome
• This is caused by ingestion of large amounts of antacids (ie. bicarbonate equivalents)
• Unlike most patients with a chloride-responsive metabolic alkalosis, these patients usually have a
high urinary Cl (ie. >20mmol/L)
o Massive PRBC transfusion

• The citrate in PRBCs is metabolized to HCO3

• Treatment of chloride-responsive metabolic alkalosis involves:
o Volume replacement with normal saline.
• This replaces both chloride and volume
• Once Cl- levels are repleted, this allows the body to excrete HCO3-
• Excretion of HCO3- corrects the metabolic alkalosis
o Adjunctive treatments for very severe alkalosis can potentially include:
• Acetazolamide
• Dialysis
• Intravenous HCl (rarely used)
Chloride-resistant metabolic alkalosis

• This is caused by excessive aldosterone activity.
o Excessive aldosterone activity causes hypokalemia.
o The drop in serum K+ leads to compensatory K+ retention by the kidney.
• -This, in turn, leads to H+ excretion by the kidney (via the H+/K+ antitransporter)
• These patients typically have a urinary Cl >20mmol/L.
• Specific etiologies of chloride-resistant metabolic alkalosis include:
o Primary hyperaldosterinism (aka “Conn’s syndrome”)
o Secondary hyperaldosterinism
o Primary hyper-reninism
o Black licorice (ie. real licorice--not the candy; acts like aldosterone)
o Congenital adrenal hyperplasia
o Excessive ACTH
• Severe hypercalcemia, hypomagnesemia, or hypokalemia
• Chloride-resistant metabolic alkalosis does not respond to normal saline.
• Instead, treatment involves:
o Fixing the underlying etiology
o Correcting any electrolyte abnormalities
o +/- Spironolactone (an aldosterone antagonist)
Approach to Acid-Base Disorders

Overview
• First question -- Is this a primary acidosis or alkalosis (ie. which side of 7.40)?
o Remember that the body almost never fully compensates for a primary acid-base disorder
• Second question -- Is this a primary respiratory or metabolic abnormality?
o What is causing the primary abnormality--the CO2 or the HCO3?
• Third question -- Is the primary abnormality appropriately compensated?
o Use the rules above to calculate appropriate compensation for the primary abnormality.
o If the primary abnormality is metabolic acidosis, start by checking the anion gap
o If the primary abnormality is anything else, check the anion gap last

o If the primary abnormality is not appropriately compensated, this suggests multiple acid-
base disorders.
• Fourth question -- If a metabolic acidosis is present, is it isolated?
o This question can be answered in two ways...
o #1 -- By understanding that:
 With an isolated AG-metabolic acidosis, the rise in AG is about the same as the fall in
HCO3
 With an isolated non-AG metabolic acidosis, the rise in Cl is about the same as the
fall in HCO3
o #2 -- By uing the Delta gap
 The Delta Gap = (AG - 12mmol/L) - (24mmol/L - HCO3)
 A normal delta gap is -6mmol/L to 6mmol/L
 A delta gap > 6 suggests a metabolic alkalosis
 A delta gap < -6 suggests a non-AG metabolic acidosis

Sample question
A 45-year-old lady presents to hospital in DKA. She has been vomiting for several days. She looks unwell.
Her bloodwork is below. What acid-base disorder(s) is/are present?
a. ABG 7.46 / 41 / 77 / 30
b. Lytes Na 139 / K 3.3 / Cl 86 / HCO3 30
1) Determine the primary acid-base abnormality.

Metabolic alkalosis (ie. the pH is >7.40; this is being caused by the increased HCO3)
2) Determine the primary abnormality is appropriately compensated.
a. Using the Marino compensation rule for primary metabolic alkalosis:
-Expected PCO2 = 0.7(HCO3) + 21 = 42
b. Since the expected PCO2 is very close to the actual PCO2 (ie. 41), respiratory compensation for the
metabolic alkalosis is appropriate.
3) Check the anion gap.
a. The AG is 23.
b. Since an elevated AG is present, the patient must also have a metabolic acidosis.
c. Therefore, at least two acid-base disorders are present (ie. metabolic alkalosis and increased-AG
metabolic acidosis)
4) Since a metabolic acidosis is present, check if it is isolated?
a. With an isolated AG metabolic acidosis, the rise in the AG should be about the same as the drop in
HCO3.
-In our patient, this is definitely not the case
-The rise in AG is 11
-Instead of a drop in HCO3, she actually has a rise in HCO3 of 6
-This extra HCO3 confirms that a metabolic alkalosis is also present
b. This can be also be done using the Delta Gap
= (AG - 12mmol/L) - (24mmol/L - HCO3)
= (23-12) - (24-30)
= 11 - (-6)
= 17
A delta gap >6 confirms the presence of a metabolic alkalosis
5) As discussed above, an increased-AG metabolic acidosis and a metabolic alkalosis can co-exist.
-They do not cancel each other out
6) In conclusion, therefore, this patient has a double acid-base disorder:
a. Metabolic alkalosis -- Secondary to vomiting
b. Metabolic acidosis -- Lactic acid from hypovolemia/hypoperfusion; ketoacids from DKA

Sepsis
Definitions
• Sepsis is defined as the presence (probable or documented) of infection together with systemic
manifestations of infection.
• Severe sepsis is defined as sepsis plus sepsis-induced organ dysfunction or tissue hypoperfusion
• Sepsis-induced hypotension is defined as a systolic blood pressure (SBP) < 90mm Hg or mean
arterial pressure (MAP) < 70mm Hg or a SBP decrease > 40mm Hg or less than two standard
deviations below normal for age in the absence of other causes of hypotension.
• Septic shock is defined as sepsis-induced hypotension persisting despite adequate fluid
resuscitation.
• Sepsis-induced tissue hypoperfusion is defined as infection-induced hypotension, elevated lactate,
or oliguria (Urine output < 0.5 ml/kg/hour)
3 hour Bundle
TO BE COMPLETED WITHIN 3 HOURS OF TIME OF PRESENTATION
1. Measure lactate level
2. Obtain blood cultures prior to administration of antibiotics
3. Administer broad spectrum antibiotics
4. Administer 30ml/kg crystalloid for hypotension or lactate ≥4mmol/L
6 hour Bundle
TO BE COMPLETED WITHIN 6 HOURS OF TIME OF PRESENTATION
1. Apply vasopressors (for hypotension that does not respond to initial fluid resuscitation) to maintain a
mean arterial pressure (MAP) ≥65mmHg
2. In the event of persistent hypotension after initial fluid administration (MAP < 65 mm Hg) or if initial
lactate was ≥4 mmol/L, re-assess volume status and tissue perfusion
3. Re-measure lactate if initial lactate elevated.
Documentation
DOCUMENT REASSESSMENT OF VOLUME STATUS AND TISSUE PERFUSION WITH:
1. Either repeat focused exam (after initial fluid resuscitation) by licensed independent practitioner
including vital signs, cardiopulmonary, capillary refill, pulse, and skin findings.
2. OR TWO OF THE FOLLOWING:
a) Measure CVP
b) Measure ScvO2
c) Bedside cardiovascular ultrasound
d) Dynamic assessment of fluid responsiveness with passive leg raise or fluid challenge

Antiboitics
Renal Dosing
1. In patients with renal failure (even if severe), the first dose of antibiotics should not be renally-dosed.
a. This is especially important if the patient is very sick
b. Renal-dosing for subsequent doses can be worked out on the ward
2. The following antimicrobials do not require renal-dosing:
a. Cloxacillin
b. Ceftriaxone
c. Cefixime
d. Erythromycin and Azithromycin (ie. Clarithromycin does)
e. Moxifloxacin
f. Doxycycline
g. Clindamycin
h. Metronidazole
Bactericidal vs. Bacteriostatic antibiotics

1. Bactericidal antibiotics include:
a. Beta-lactams (eg. penicillins, cephalosporins, carbapenems)
b. Fluoroquinolones
c. Aminoglycosides
d. Vancomycin (slowly bactericidal)
e. Metronidazole
2. Bacteriostatic antibiotics include:
a. Macrolides
b. Clindamycin
c. Linezolid
d. Tetracyclines
3. The clinical significance of bactericidal over bacteriostatic antibiotics remains controversial.
4. Nontheless, as of 2014, bactericidal agents are indicated for most serious infections (eg. bacteremia,
endocarditis, meningitis)
Penicillins
Overview
1. The penicillins include:
a. Natural
b. Beta-lactamase-resistant (ie. anti-staphylococcal)
c. Aminopenicillins (ie. extended-spectrum)
d. Anti-pseudomonal
e. Associated with beta-lactamase inhibitors
2. The penicillins are beta-lactam antibiotics.

a. They are bactericidal

Natural penicillins
1. These include:
a. Pen G (parenteral)
b. Pen V or VK (oral)
c. Benzathine penicillin
2. These agents are generally:
a. Active against:
i) Many Strep species
ii) Oral anaerobes (eg. peptostreptococcus, +/- Bacteroides)
iii) Many GPBs (eg. Anthrax, Clostridium, Listeria, +/- Enterococcus)
b. Not active against:
i) Beta-lactamase organisms
c. Staph species
Beta-lactamase-resistant (aka penicillinase-resistant) penicillins

1. These include:
a. Cloxacillin
b. Methicillin
2. These agents are generally:
a. Active against:
i) Strep species
ii) Staph aureus (ie. MSSA, not MRSA)
b. Not active against:
i) MRSA
ii) Most strains of coagulase-negative staph (ie. usually only sensitive to Vancomycin)
iii) Enterococcus
iv) Gram-negatives
v) Anaerobes
For non-Staph/Strep infections, the other penicillins are preferred.
Aminopenicillins (ie. extended-spectrum)

1. These include:
a. Ampicillin
b. Amoxicillin
2. These agents offer some GP and GN coverage:
a. Strep species
b. +/- Enterococcus fecalis (but not E. fecium)
c. E. coli
d. H. flu
e. Salmonella
f. Listeria
g. Proteus

3. The mnemonic is “SHEPS” (Salmonella, H. flu, E. coli, Proteus, Shigella)
Anti-pseudomonal penicillins
Pipercillin
1. This covers
a. Strep species (but not as well as some of the other penicillins)
b. E. fecalis (not E. fecium)
c. Some anaerobes
d. Pseudomonas
e. Many Enterobacteraciae (eg. E. coli, Klebsiell)
2. Pipercillin is commonly combined with Tazobactam (see below), to provide even broader coverage.
a. Ticarcillin
b. Carbenicillin
Pencillins associated with beta-lactamase inhibitors

Pip-Tazo (ie. Pipercillin-Tazobactam)
1. Pipercillin is the antibiotic; Tazobactam is the beta-lactamase inhibitor
2. Pip-Tazo is a "big gun" antibiotic.
3. It covers a broad ranges of GP's, GN's (including Pseudomonas), and anerobes.
4. Pip-Tazo does not cover atypicals (ie. Mycoplasma pneumoniae, Legionella, Chlamydophlia
pneumoniae).
5. As such, additional antibiotic coverage is needed for patients with community-acquired pneumonia (eg.
macrolide, fluoroquinone, doxycycline)
6. Clavullin (ie. Amoxil-Clavullinic acid)
7. Tic-Clav (ie. Ticarcillin-Clavullinic acid)
Cephalosporins
The cephalosporins are beta-lactam antibiotics. The first three generations of cephalosporins do not cover:
a. Anerobes
b. Enterococcus
In general:
a. First-generation cephalosporins cover more GP's, but some GN's
c. Second-generation cephalosporins cover some GP's and some GN's
b. Third-generation cephalosporins cover more GN's, but some GP's
The mnemonic for gram-negative coverage of the cephalosporins is as follows:

a. 1st-generation -- PEK (Proteus, E. coli, Kleb)
b. 2nd-generation -- H-PEK (Hemophilus, Proteus, E. coli, Kleb)
c. 3rd-generation -- HEN-PEK (Hemophilus, Enterobacteriaceae, Neisseria, Proteus, E. coli, Kleb)
1st-generation cephalosporins
a. These include Cefazolin and Cephalexin

b. GP coverage includes Strep species, MSSA

c. GN coverage includes PEK
2nd-generation cephalosporins
a. These include Cefuroxime and Cefoxitin
b. GP coverage includes Strep species, MSSA
c. GN coverage includes H-PEK, Moraxella
3rd-generation cephalosporins
a. The IV agents include Cefotaxime, Ceftriaxone, Ceftazidime
b. The PO agents include Cefixime
c. GP coverage includes Strep, +/- MSSA (if high-dose given)
d. GN coverage includes HEN-PEK, most GN's, and Ceftazidime covers Pseudomonas
-While Ceftazidime cover Pseudomonas, it has worse GP coverage than the other 3rd-gens
Be aware that there are three different dosing regimens for Ceftriaxone:
a. For uncomplicated pneumonia -- 1g IV q24h
b. For suspected bacteremia or endocarditis -- 2g IV q24h
c. For suspected meningitis -- 2g IV q12h
As mentioned, Ceftriaxone does not require renal dosing.
Aminoglycosides
These include:
a. Amikacin
b. Streptomycin
c. Gentamicin
d. Tobramycin
Lung penetration of the aminoglycosides is poor.

-As such, these agents should not be used for pneumonia
The aminoglycosides have broad GN coverage--including Pseudomonas (especially Tobramycin)
GP coverage is poor to non-existent.
Extended-dosing of Gentamicin and Tobramycin (ie. 7mg/kg q24-48h) has replaced conventional dosing (ie.
2mg/kg q8h) for most indications.
The aminoglycosides are commonly avoided because of fears of causing renal failure.
a. While this is a significant concern with prolonged use, it is extremely rare with one-time use
b. As such, for patients with severe sepsis of unclear etiology, consider giving a one-time dose of
Gentamicin or Tobramycin to provide broad gram-negative coverage for 24-48 hours

Fluoroquinolones
These include:
a. Ciprofloxacin
b. Levofloxacin
c. Moxifloxacin
Fluoroquinolones (like macrolides) can prolong the QTc.
The fluoroquinolones cover:

a. Most GN's
b. Atypicals
c. Some GP's (ie. Levo and Moxi only)
d. Some anerobes (ie. Moxi only)
Ciprofloxacin
a. This has good gram-negative coverage (including N. gonorrhea, H. influenzae, and Pseudomonas)
-Pseudomonal coverage with the other fluoroquinolones is less reliable
b. Ciprofloxacin does not cover any anerobes.
Levofloxacin
a. This has better gram-positive coverage than Cipro (ie. mainly Strep species)
b. It covers most GNs, but its coverage of Pseudomonas is unreliable
c. It also does not cover any anerobes
Moxifloxacin
a. This has quite broad-spectrum coverage, including:
-Strep and Staph species
-Most GNs, but not Pseudomonas
-Anerobes
b. Be aware that Moxifloxacin does not penetrate into the urinary system.
-As such, it should not be used for urinary infections
Macrolides
These include:
a. Erythromycin
b. Clarithromycin
c. Azithromycin
These agents are bacteriostatic, not bactericidal.
Macrolides (like fluoroquinolones) can prolong the QTc.

The macrolides all have grossly similar coverage, including:

a. Strep species
b. H. influenzae (Azithro ≥ Biaxin > Erythro)
c. Most atypicals
Erythromycin
a. This is active against:
-Strep species
-Atypicals
-Chlamydia and Neisseria
b. It has poor activity against H. influenzae.
c. It is not commonly used--because of its significant GI side-effects (eg. nausea).
Clarithromycin
a. This is active against:
-Strep species (including S. pneumo)
-Atypicals
-Moraxella
-H. influenzae (more than Erythro, less than Azithro)
b. It has fewer GI side effects than Erythromycin.
Azithromycin
This is active against:
-Strep species
-Atypicals
-H. influenzae
Azithromycin has a long half-life.

-As such, a 3-5 day course is adequate for most indications
Azithromycin has fewer GI side-effects than the earlier macrolides.
Metronidazole (aka Flagyl)

Metronidazole covers:
a. Most anaerobes (especially gram-negative)
b. Parasites (eg. Giardia, Entamoeba)
Metronidazole's anerobe coverage is likely superior to Clindamycin's.
Side-effects of Metronidazole include:

-Nausea
-Metallic taste
-Neuropathy
-Possible reaction with ethanol
Clindamycin
Clindamycin covers:
a. Strep species (moderate coverage)

b. MSSA (good coverage)

c. Community-acquired MRSA (although resistance rates are now quite high)
d. Anerobes
Clindamycin does not cover:

a. GN's
b. Enterococcus
Clindamycin is bacteriostatic.
It is probably the #1 cause of antibiotic-induced C. difficile.
Tetracyclines
These include:
a. Tetracycline
b. Doxycycline
c. Minocycline
d. Tigecycline
The tetracyclines are bacteriostatic.
The tetracyclines cover several unusual organisms, including:

a. Rickettsia
b. Chlamydia
c. Mycoplasma
d. Vibrio cholera
e. Brucella
f. Borreila burgdorferii (ie. Lyme disease)
Doxycycline is commonly used in the ED.
a. GP coverage includes Strep pneumoniae, and some other GP's
b. Doxycycline is somewhat unpredictable against Staph species, but covers some strains of community-
acquired MRSA (but not hospital-acquired MRSA)
c. Doxycycline reliably covers atypicals
d. It does not cover anerobes
Sulfa drugs
The most common sulfa drug in clinical use is TMP/SMX (aka Septra, Bactrim).
Septra has broad-spectrum coverage, including:

a. Streptococcus and Staphylococcus species (including community-acquired MRSA, but not hospital-
acquired MRSA)
b. H. influenza

c. Listeria
d. Many Enterobacteraciae (eg. E. coli, Klebsiella, etc.)
e. Stenotrophomonas
f. PJP
Septra does not cover Enterococcus.
Septra is contraindicated in renal failure.
Nitrofurantoin
NF is concentrated in the bladder.
a. As such, it is only indicated for lower urinary tract (ie. bladder) infections.
b. It should not be used for any upper urinary tract infections, pyelonephritis, or urosepsis
NF is contraindicated in renal insufficiency.For bladder infections, NF is effective against:

a. S. aureus
b. Enterococcus
c. E. coli
d. Some strains of Klebsiella
Carbapenems
The carbapenems include:
a. Imipenem
b. Meropenem
c. Ertapenem
Like Pip-Tazo, the carbapenems are "big gun" antibiotics.

a. They cover a broad ranges of GP's, GN's (including Pseudomonas), and anerobes.
b. Note that Ertapenem does not cover Pseudomonas.
Carbapenems do not cover:

a. MRSA
b. Coagulase-negative Staph
c. Atypicals (ie. additional antibiotics are needed for community-acquired pneumonia)
The carbapenems:
a. May cover Enterococcus fecalis (not Ertapenem)
b. Generally do not cover Enterococcus fecium
Ertapenem is not commonly used in the ED.
a. It has convenient once-daily dosing, but is very expensive (ie. $100/day as of 2012)
c. Unlike Imipenem and Meropenem, it has no Pseudomonal coverage
d. It also has no Enterococcus coverage

Vancomycin
Vancomycin covers:
a. Nearly all gram-positive aerobes (including MRSA, coagulase-negative Staph, Strep, Enterococcus,
Listeria, Bacillus)
b. Many gram-positive anaerobes (eg. C. difficile, peptostreptococcus)
In general, however, Vancomycin is not a great antibiotic.

a. It is inferior to beta-lactam antibiotics for treating beta-lactam-sensitive organisms.
-Therefore, if an organism is sensitive to both Vancomycin and beta-lactam antibiotics (eg. penicillins,
cephalosporins, carbapenems), choose the beta-lactam.
b. Vanco is sometimes described as being bacteriostatic, however it is slowly bactericidal in most cases.
Vancomycin remains in wide clinical use because it is a first-line antibiotic for:

a. MRSA
b. Coagulase negative Staph
c. Enterococcus (especially E. fecalis, +/- E. fecium)
-Vancomycin obviously does not cover VRE (ie. Vancomycin-resistant enterococcus)
Linezolid
1) Linezolid is a bacteriostatic antibiotic.
-It can be given PO or IV
2) It is effective against many GP's:

a. MSSA
b. MRSA
c. Strep species (including Strep pneumo, Group A Strep)
d. Enterococcus fecalis (including VRE), +/- E. fecium
3) It has no activity against gram-negatives.
4) Linezolid is typically used:

a. As a second-line agent for MRSA (ie. if resistant to Vancomycin)
b. As a first-line agent for VRE

Inotropes
Definitions
1. Inotropes increase cardiac contractility.

2. Chronotropes increase heart rate.
3. Inotropes can have positive chronotropic effects (eg. epinephrine, NE, Dop, Dob), negative
chronotropic effects (eg. digoxin), or minimal chronotropic effects (eg. Milrinone)
4. Vasopressors cause contraction of blood vessels.
5. Vasopressors generally cause an increase in blood pressure
6. However, an increase in BP does not necessarily correlate with an increase in end-organ perfusion
Adrenergic Receptors
There are several types of adrenergic receptors:
1. Alpha-1 -- Activation of this post-synaptic receptor causes peripheral vasoconstriction.

2. Alpha-2 -- Pre- and post-synaptic activation of this receptor causes a variety of effects which are
difficult to characterize from an inotropic/vasopressor standpoint.
3. Beta-1 -- Activation of these receptors increase cardiac inotropy and chronotropy.
4. Beta-2 -- Activation of these receptors in the:
a. Lung causes bronchodilation
b. Peripheral blood vessels causes peripheral vasodilation
Commonly-Used Inotropes
Summary
The following agents can be characterized in terms of their inotropic, chronotropic, and
vasoconstrictive/vasodilative properties as follows (ie. if a property is not listed, it is assumed to be zero)
1. Epi (1-20ug/min)
a. 4+ inotropy
b. 4+ chronotropy
c. 4+ vasoconstriction
2. NE (1-20ug/min)
a. 2+ inotropy
b. 1+ chronotropy
c. 4+ vasoconstriction
3. Dopamine
a. 1-4ug/kg/min
b. 1+ inotropy
c. 1+ chronotropy

d. 1+ vasodilation
4-20ug/kg/min
e. 2+ inotropy
f. 2-3+ chronotropy
g. 2-3+ vasoconstriction (ie. increasing vasoconstriction with increasing dose)
4. Dobutamine (2-20ug/kg/min)
a. 3-4+ inotropy
b. 1-2+ chronotropy
c. 2+ vasodilation
5. Milrinone (0.125-0.5ug/kg/min)
a. 4+ inotropy
b. No chronotropy (unlike Dobutamine)
c. 3+ vasodilation (although the risk of hypotension is lowered by avoiding an initial bolus
dose)
Details
1. Epinephrine ("Epi")
a. Epinephrine is an endogenous catecholamine synthesized in the adrenal medulla from the
amino acids phenylalanine and tyrosine.
b. Action: +++B1, ++B2, +++a1
c. Epi causes profound inotropy, chronotropy, and vasoconstriction. Its vasodilatory B2-activity
is more than outweighed by its vasoconstrictive a1-activity
d. Epinephrine can be a useful agent for undifferentiated hypotension, but can have several
troublesome side-effects:
 Hyperglycemia (even in non-diabetics)
e. Metabolic acidosis (ie. often down to a serum HCO3 17–21meq/L; usually self-limited)
2. Norepinephrine (“Levophed”, "Nor-Ad")

a. Norepinephrine is also an endogenous catecholamine synthesized in the adrenal medulla
from tyrosine.
b. Action: ++B1, +B2, +++ a1
c. Like Epi, NE's vasodilatory B2-activity is more than outweighed by its vasoconstrictive a1
activity
d. While NE has a significant inotropic component, it tends to cause less chronotropy than
many other inotropes (eg. epi, +/- Dopamine, +/- Dobutamine)
e. As such, it may be a useful agent in patients with undifferentiated hypotension who are
tachycardic
f. Over the past ten years, NE has become a favoured agent in septic shock.
3. Dopamine ("Dop")
a. Like Epi and Norepi, Dopamine is a physiological catecholamine.
b. From an inotropic standpoint, Dopamine acts indirectly--promoting release of the body's
own endogenous catecholamines

c. Dopamine is more difficult to characterize from an inotropic/pressor standpoint because:

d. It primarily stimulates dopamine receptors
e. It has differing hemodynamic effects at different infusion rates
f. Dopamine can be run at:
1. 0.5-3 ug/kg/min (low dose) -- Predominantly affects the dopamine receptors;
possible selective vasodilation in certain visceral circulation
2. 3-10 ug/kg/min (moderate dose) -- Moderate B1 and mild a1 activity
3. 10-20ug/kg/min (high dose) -- Steadily-increasing a1 activity
g. Dopamine has prominent chronotropic activity--and can cause tachycardia +/-
tachyarrhymias.
h. At moderate doses, Dopamine acts as a diuretic (via a carbonic-anhydrase-inhibitor

mechanism).
i. Although this effect was previously believed to improve renal function in ARF, this notion of
"renal-dose Dopamine" has since been debunked
j. Patients maintained on Dopamine infusions for several days can have pituitary inhibition
(eg. inhibition of PRL, TSH, LH)
4. Dobutamine (“Dobutrex”, "Dob")

a. Dobutamine is a synthetic agent.
b. Action: +++B1, +B2, +a1
c. It is typically given at a rate of 2.5 (low-dose) to 20 (high-dose) ug/kg/min.
d. Dobutamine acts an inotrope, a moderate chronotrope, and a vasodilator.
e. The chronotropic effect of Dobutamine (which is not seen with Milrinone) can be beneficial
or detrimental depending on the clinical setting
f. In addition to its cardiac effects, Dobutamine causes peripheral vasodilation--with up to 33-
50% of patients having a decrease in blood pressure when started on Dobutamine
g. Therefore, while Dobutamine is a useful agent for cardiogenic shock (especially in
bradycardic patients), it is generally not beneficial (or even harmful) for other forms of
shock.
5. Milrinone
a. Milrinone is a phosphodiesterase inhibitor.
b. It effects include:
c. Increased inotropy without increased chronotropy
d. Enhanced lusitropy (ie. cardiac relaxation during diastole)
e. Pulmonary and systemic vasodilation
f. Milrinone toxicity manifests as cardiac dysfunction.
g. Milrinone is renally-cleared, and a lower-dose should be used in renal failure
h. Clinically, Milrinone can be used is similar settings to Dobutamine--especially if additional
chronotropy is not desireable.
i. As such, Milrinone is a useful agent for cardiogenic shock (especially in tachycardic patients),
but is generally not beneficial (or even potentially harmful) for other forms of shock

Cardiac Emergencies
Contents
Myocardial Infraction....................................................................................................................................... 68
Signs and Symptoms .................................................................................................................................... 68
Electrocardiography ..................................................................................................................................... 68
Q wave based criteria .............................................................................................................................. 68
ECG finding prediciting Culprit Coronary Artery...................................................................................... 68
Cardiac Enzymes .......................................................................................................................................... 69
Management ................................................................................................................................................ 69
PCI ................................................................................................................................................................ 70
Arrhythmias ..................................................................................................................................................... 72
Types of tachyarrhythmia: ........................................................................................................................... 72
Types of Brady Arrhythmia .......................................................................................................................... 73
Investigations ............................................................................................................................................... 73
Management ................................................................................................................................................ 74
Cardiogenic Shock ............................................................................................................................................ 76
Causes of cardiogenic shock ........................................................................................................................ 76
Clinical features............................................................................................................................................ 76
Investigations ............................................................................................................................................... 76
Management ................................................................................................................................................ 76
Acute Pulmonary Oedema ............................................................................................................................... 78
Introduction ................................................................................................................................................. 78
Investigations ............................................................................................................................................... 78
Management ................................................................................................................................................ 78
Hypertensive Crisis........................................................................................................................................... 79
Myocardial Infraction
Signs and Symptoms
Features High Likelihood Intermediate Low Likelihood
Likelihood
History Chest of left arm discomfort as chief Chest of left arm Probable ischemic
complaint reproducing prior discomfort as chief symptoms in absence of
documented angina complaint any of the intermediate
Previous history of CAD Age more than 70 years likelihood
Male sex characterstics
DM Recent cocain use
Examination Transient MR, Hypotension, Extracardiac Vascular Chest discomfort
Diaphorresis, Pulmonary Oedema or Disease reproduced by
Rales palpation
ECG New or presumable new, transient Fixed Q waves T wave flattening or
ST segment deviation (1 mm of ST depression 0.5 or 1.0 inversion <1 mm in
greater) or T wave inversion in mm or T wave inversion leads with dominant R
multiple precordial leads > 1mm waves
Cardiac Elevated cardiac troponin I or CPK Normal Normal
Markers MB
Electrocardiography
Q wave based criteria
Location Electrocardiography
Anteroseptal QS deflection in V1, V2, V3 and possibly V4
Anterior Rs deflection in V1 and Q WAVES IN V2-V4 or decrease in amplitude of initial R
waves in V1-V4
Anterolateral Q waves in V4-V6, I and avl
Lateral Q waves in I and avl
Inerior Q waves in II, III, avf
Interolateral Q waves in II, III, avf, V5 and V6
True posterior Initial R waves in V1 and V2 ? 0.04 sec and R/S ≥1
Right Ventricular Q waves in II, III, avf, and ST elevation in right side V4
ECG finding prediciting Culprit Coronary Artery

Culprit artery ECG Finding
ECG findings fof inferior ST segment elevation MI
Right Coronary ST segment elevation in lead III greater than lead II plus ST segment depression of >
Artery 1 mm in lead I , avl or both
Proximal right In addition to the findings immediately above ST segment elevation on V1, V4R or
coronary artery both
Left circumflex Absence of the above findings plus ST segment elevation in leads I, avl, V5, V6 and
artery ST segment depression in leads V1, V2 and V3

ECG findings for anterior ST segment dlevation MI

ST segment elevation inleads V1, V3 and V3 plus any of the features below
Proximal left ST segment elevation of more than 2.5mm in lead V1 or RBBB with Q wave or both
anterior
descending artery
Proximal left ST segment depression of > 1 mm in lead II, III, avf
anterior
descending artery
Distal let anterior ST segment depression of ≤ 1 mm or ST segment elevation in leads II, III and avf
descending artery
Cardiac Enzymes
Enzyme Onset Peak Duration
CPK MB 3-12 hours 18-24 hours 36-48 hours
Troponin I 3-12 hours 18-24 hours Up to 10 days
Send Na, K, Createnine (other investigations as relevant)
Management
1. Aspirin 300 mg PO
2. Clopidogrel 300 PO
3. Enoxaparin 30 mg IV bolus or Heparin 60 U/kg (Maximum 4000 U)
4. Morphine 2-5 mg IV every 5-15 minutes PRN pain
5. Nitroglygerine 0.6 mg every 4 min x 3 PRN pain or IV start at 10 microgram/min titrate to 10% reduction of
MAP in normotensive and 30% reduction of MAP if hypertensive
a. Contraindications: Right ventricular ischaemia, Hypotension
6. Metoprolol 50 mg PO 12 hourly on first day or if significant HTN 5 mg over 2 mins iv every 5 mins up to 15
mg
a. Contraindiation: Hypotension
7. Streptokinase
a. Indication: Patient with STEMI if time to treatment is <6 hours to 12 hours from symptom onset and
ECG has lt least 1 mm ST elevation in two or more contiguous leads.
b. Contraindications:
i. Absolute
1. Any prior intracranial hemorrhage
2. Known structural cerebral vascular lesion
3. Known intracranial neoplasm
4. Ischemic stroke within 3 months
5. Active internal bleeding
6. Suspected aortic dissection of pericarditis
ii. Relative contraindication
1. BP >180/100 mmhg
2. History of chronic severe poorly controlled HTN
3. History of prior stroke more than 3 month or known intracranial pathology not
covered in contraindication
4. Current use of anticoagulants with known INR >2-3
5. Bleedign diasthesis

6. Trauma in last 2 weeks

7. Prolonged CPR (more than 10 mins)
8. Major surgery < 3weeks
9. Non compressible vascular puncture
10. Recent internal bleeding 2-4 weeks
11. Previously treated with STK
12. Pregnancy
13. Active peptic ulcer bleeding
PCI
STEMI within 90 minutes
Non STEMI within first 48 hours
Indications
1. Recurrent angina or ischemia with or without CHF
2. Elevated cardiac enzymes
3. New or presumly new ST depression
4. High risk findins in non invasive stress test
5. Deperssed left ventricular function
6. Hemodynamic instability
7. Sustained let ventricular tachycardia
8. PCI within last 6 month or previous CABG

Chest pain suggestive of ACS
ECG
ECG changes suggestive of STEMI No ECG Changes
Cardiac enzymes to be sent
Positive
Emergency Management CPK MB/Troponin
1. ABCDE
Negative
2. Cardiac monitor
3. Oxygen
4. IV line If pain still persistent
5. Aspirin 300mg Positive Rule out other causes
ECG or Repeat ECG at 30 mins
6. Nitrates (if not contraindicated)
Cardiac Repeat cardiac enzyme at 4 hours
7. Morphin
Enzymes
8. Metoclopramide/ Promethazine
Negative
TIMI score
1. Age ≥ 65
Admission in Cardiac Unit
High Risk 2. Presence of at least three risk
factor of coronary heart disease
3. Prior coronary stenosis of ≥ 50%
4. Presence of ST segment
deviation on admission ECG
5. Elevated serum cardiac
biomarkers
6. At least two angina episodes in
prior 24 hours
7. Use of aspirin in prior seven days
0-1: low risk, 2-3: intermediate risk, 4-7
high risk
Low or Intermediate risk
Yes
Chest pain even after primary management
No
Discharge

Arrhythmias
Tachyarrhythmia (HR > 120bpm) and bradyarrhythmias (HR < 60bpm) may present with significant
symptoms and hemodynamic compromise.
Types of tachyarrhythmia:
Tachyarrhythmia
Narrow complex Tachyarrhythmia Broad complex Tachyarrhythmia

QRS complex ≤ 3 small squares QRS complex > 3 small squares
Regular Rhythm Irregular Rhythm Regular Rhythm Irregular Rhythm

1. Sinus Tachycardia Atrial Fibrillation Ventricular Tachycardia AF, atrial flutter with BBB
2. Atrial flutter
3. PSVT
Sinus Tachycardia: A sinus rate more than 100 per minute usually due to increase in sympathetic activity
associated with exercise, emotion stress, fever and variety of other pathological conditions (Heart failure,
thyrotoxycosis etc)
Atrial Flutter: There is rapid atrial rate around 250-300/min. The ECG shows characteristics saw toothed
flutter waves.
Atrial fibrillation: In this arrhythmia the atrial beat is 350 to 500 bpm and ventricular response at irregular
intervals. ECG shows irregularly irregular rhythm.
Paroxysmal Supraventricular Tachycardia (PSVT): This rhythm is due to re-entry within the AV node or
accessory pathway and produces regular tachycardia.

Ventricular tachycardia: This is a grave arrhythmia usually associated with serious heart disease and may
be degenerated into ventricular fibrillation (This produces rapid ineffective uncoordinated contraction of
the ventricles)
Types of Brady Arrhythmia

Sinus Bradycardia: Sinus rhythm less than 60 beats per minutes
Heart Block: Pathological non conduction of atrial impulse to ventricle due to the block at AV node or HIS
system.
1. First degree AV block: Delayed conduction through AV node. ECG shows prolong PR interval which
is more than 0.20 seconds.
2. Second degree AV block
a. Type I: There is gradual prolongation of PR interval till one P fails to conduct to the ventricle.
b. Type II: There is sudden non conduction of an atrial impulse to the ventricle.
3. Third degree AV block: Complete absence of conduction of atrial impulse to the ventricle. ECG
shows AV dissociation with escape junctional or ventricular rhythm.
Clinical feature Causes of Arrhythaemia

1. Palpitations 1. Ischemic heart disease,
2. Chest pain 2. Cardiomyopathies
3. Breathlessness 3. Valvular Heart Disease
4. Collapse or hypotension 4. Hypertension, Heart failure
5. Embolic event like stroke 5. Pericarditis
6. Endocarditis
7. Myocarditis
Investigations
8. Pneumonia
• ECG 9. Pulmonary embolus
• Chest X ray: Cardiomegaly, pulmonary oedema 10. Trauma
• Electrolytes: Hypokalaemia, renal impairments 11. Electrolytes disturbance
• Cardiac Enzymes 12. Acidosis
13. Thyrotoxicosis
14. Alcohol

Management
1. Secure ABC
2. Give oxygen
3. Secure peripheral venous line
4. Put patient in cardiac monitor
5. If hemodyamically unstable catheterize the patient
Arrhythmia
Broad Complex Tachycardia Narrow Complex Tachycardia
Treat as VT unless otherwise proved

Supraventricular Tachycardia
Ventricular Tachycardia
Unstable patient
Synchronized DC shock
200 Joules
Hemodyamically Unstable Hemodyamically Stable
Unsynchronized DC shock Chemical cardioversion

360 Joules Amiodarone Stable Patient
Loading dose: 300mg iv
over 60 minutes followed
by 900mg iv over 23 hours
 200 mg po tds for 1 Regular Rhythm: PSVT Irregular Rhythm: AF,
week 200mg po bd for 1 •Vagotonic Maneuvers Atrial Flutter
week •Inj Adenosine 6mg
Maintenance dose: 200- iv9mg iv 12mg iv
400mg od iv or po •Digoxin, Calcium
channel blocker >48 Hours < 48 Hours
(should be avoided in •Ventricular Anticoagulatio
AVRT: eg WPW Rate Control: n at
syndrome*), Beta Beta blocker, presentation
Blocker digoxin, CCB with LMWH or
•If there is •Heparin (UFH) UFH followed
degeneration of the 5000 IU by chemical
rhythm into a broad followed by cardioversion
complex infusion or with
tachyarrhythmia and LMWH Amiodarone
or hemodyamically •Sinus rhythm
compromise  control with
electrical amiodarone
cardioversion later

Bradycardia
Hemodyamically Unstable Hemodyamically Stable
Cardiac Arrest, Asystole, SBP < 90mmHg, Severe Admit to CCU

Pulmonary Oedema, Evidence of Cerebral
f
Immediate Management:
•Atropine 1mg iv bolus; repeat if
necessary upto maximum 3 mg
•Isoprenaline 0.2mg iv if there is
delay in pacing and the patient
remains unstable. Set up an
infusion (1mg in 100 ml NS
starting at 1ml/min titrating to
heart rate)
•Start percutaneous cardiac pacing
and send to cardiac centre

Cardiogenic Shock
Cardiogenic shock is a clinical condition of inadequate tissue (end-organ) perfusion due to cardiac
dysfunction.
Causes of cardiogenic shock

• Myocardial Infraction (MI)
• End stage cardiomyopathy
• Myocarditis
• Septic shock with severe myocardial depression
• Left ventricular outflow obstruction: Aortic stenosis, Hypertrophic obstructive cardiomyopathy
• Obstruction to left ventricular filling: Mitral stenosis
• Acute mitral regurgitation
• Myocardial contusion
Clinical features
• Hypotension
• Tachycardia
• Olyguria
• Cool periphery
• Respiratory Distress
• Jugular venous distention
Investigations
• ECG
• Cardiac Enzymes
• Complete blood count: Leukocytosis is common
• Sodium, Potassium, Creatinine
Management
1. Secure ABC
2. Give oxygen
3. Secure peripheral venous line
4. Send investigations
5. Put patient in cardiac monitor
6. Catheterize the patient
7. Correct Reversible factor
• Arrhythmias
• Electrolyte and acid base disturbances
• Ventilation abnormalities: Intubate if necessary
8. Aim to improve hemodynamic status achieving SBP≥ 90mmhg
IV fluid (with caution), Inotropic support ± diuretics

Cardiogenic shock
Hypotensive Non Hypotensive
Dopamine (Upto 20µgm/kg/min) Dobutamine (Upto 20µgm/kg/min)

Noradernaline (Upto 20µgm/kg/min) Noradernaline (Upto 20µgm/kg/min)
Diuretics according to clinical condition Diuretics (Frusemide)
Vasopressors are indicated for a decrease of >30 mmhg from baseline systolic blood pressure, or a mean arterial
pressure <60 mmhg when either condition results in end-organ dysfunction due to hypoperfusion. Hypovolemia
should be corrected prior to the institution of vasopressor therapy.

Acute Pulmonary Oedema
Introduction
Increase in lung fluid secondary to leakage from pulmonary capillaries into the interstitium and alveoli of
the lung
Clinical features
• Weakness, fatigue, anxiety, cold skin
• Dyspnea, Orthopnea, paroxysmal nocturnal Dyspnea
• Cough: Pink frothy sputum
• Tachypnea, wheeze, ronchi, crepitations, Intercostal retractions
• Tachycardia, JVP distention
Investigations
• Chest x ray: Effusions, butterfly infiltrates
• ECG
• Complete blood count
• Electrolytes and creatinine
Management
• Secure ABC
• Keep upright position
• Check oxygen saturation and bedside blood sugar
• Give oxygen via mask
• Secure intravenous access
• Send blood for investigations
• If BP is >150/100 mmhg nitroglycerine 0.2-0.4/kg/min and IV Furosemide
• If BP is low start Dopamine
• Inform ICU

Hypertensive Crisis
Blood pressure ≥220/120 mmHg
Without end organ damage With end organ damage
Hypertensive Urgency Investigations Hypertensive Emergency

Malignant Hypertension
ECG Headache, visual change, nocturia,
Blood sugar chest pain, papilledema
Createnine Hypertensive Encephalopathy
Electrolytes Nausea, vomiting, disorientation.
For proven hypertensive CT head (if needed) Altered mental status, seizure
Urgency maintain BP <160/80
mmHg within days to week so
can be discharged on oral
Initial fall of BP not exceeding
medication
25% of initial value in 4-6 hr
Diastolic BP not less than
Nifedipine SR 10 mg orally 100mmHg in 4-6 hour
Not controlled
after 1 hour
Repeat Nifedipine SR 10 mg orally
Not controlled
after 1 hour
Repeat Nifedipine SR 10 mg orally
1 hour
Inform ICU/Step Down

Nitroprusside: 0.25 to
0.5 µg/kg per min;
maximum dose: 8 to 10
µg/kg per min.

Respiratory Emergencies
Contents
Chest Pain ........................................................................................................................................................ 80
Pulmonary Embolism ....................................................................................................................................... 80
Shortness of Breath ......................................................................................................................................... 81
Hemoptysis ...................................................................................................................................................... 82
Acute Exacerbation of Chronic Pulmonary Obstrutive Disase ........................................................................ 83
Diagnosis nomenclature .............................................................................................................................. 83
Diagnosis, Initial Assessment and Investigations ........................................................................................ 83
Management ................................................................................................................................................ 83
Disposition ................................................................................................................................................... 84
Stable Chronic Obstrutive Pulmonary Disease ................................................................................................ 87
Diagnosis nomenclature .............................................................................................................................. 87
Diagnosis ...................................................................................................................................................... 87
Clinical Findings............................................................................................................................................ 87
Pulmonary function test .............................................................................................................................. 87
Management ................................................................................................................................................ 88
Follow up...................................................................................................................................................... 89
Bronchial Asthma ............................................................................................................................................. 90
Introduction ................................................................................................................................................. 90
Investigations ............................................................................................................................................... 90
Management ................................................................................................................................................ 90
Discharge medication ...................................................................................................................................... 91
Admission criteria ........................................................................................................................................ 91
Discharge criteria ......................................................................................................................................... 91
Community Acquired Pneumonia .................................................................................................................... 92
Introduction ................................................................................................................................................. 92
Clinical Features ........................................................................................................................................... 92
Investigations ............................................................................................................................................... 92
Management ................................................................................................................................................ 92
Pneumothorax ................................................................................................................................................. 94
Causes .......................................................................................................................................................... 94
Investigation................................................................................................................................................. 94
Management ................................................................................................................................................ 94
AMS/HAPE/HACE ............................................................................................................................................. 96
Chest Pain
Patient with chest
Does the patient have a typical or atypical angina

pattern, pain radiation or diaphoresis, or cardiac
No Ye
Is wells score suggestive of Pulmonary Embolism Follow flowchart for chest pain
Yes No
Investigate for Does the patient have fever
egophony or dullness/hyper
pulmonary resonant on percussion?
embolism
No Yes
Screening question for Perform chest x ray
Consider:Pneumonia, Pneumothorax
panic disorder: Positive
No Yes
Is pain reproducible by Consider Panic disorder
No Yes
Consider heart failure or gastrointestinal Consider Chest wall
Pulmonary Embolism
Wells model for clinical diagnosis of pulmonary embolism
Clinical findings Points
Clinical signs: leg swelling or pain with palpation of deep leg veins 3
PE as likely or more likely than an alternative diagnosis 3
Heart rate more than 100 beats per minute 1.5
Immobilization (bed rest except for bathroom access in 3 consecutive days), or surgery in 1.5
past four week
Previous objectively diagnosed DVT or PE 1.5
Hemoptysis 1
Malignancy 1
Total points Risk of PE Probability of PE (%)
<2 Low 1 to 28
2 to 6 Moderate 28 to 40
>6 High 38 to 91

Shortness of Breath
Patient with Shortness of Breath in Emergency
Upper airway Pulmonary Cardiac Neurological Toxic

Tracheal FB Pulmonary embolism ACS Stroke Metabolic
Angioedema COPD ADHF Neuromuscular Poisoning
Anaphylaxis Asthma Flash Pulmonary Disease Metabolic
Infection Pneumothorax2 Oedema Acidosis
Airway Trauma Pneumomediastinum High output failure DKA
Infection Cardiomyopathy Sepsis
Pulmonary Oedema Arrhythmia Anaemia
Others
Trauma Valvular dysfunction Acute Chest
Intra abdominal
Hemorrhage Cardiac Temponade Syndrome
process
Pleural Effusion
Pregnancy
Obesity
Hyperventilation/
Anxiety

Hemoptysis
Hemoptysis
Is it massive?
Massive: > 600ml per 24 hours or >300ml over 4 hours
Yes No
Initial management Hemodynamically stable

• ABC
• IV open with NS or RL (may
No Yes
need fluid resuscitation or
blood transfusion) CBC and CXR
• Oxygen
• Blood for investigation
(complete blood count,
hematocrite, blood group, Discharge on
coagulopathy) oral
• Chest x ray antibiotics if
• Catheterization (if needed) Referral for further indicated
• Place the patient in recovery urgent management
position with bleeding lung
down
• Nebulisation if needed
• Urine output monitoring

Acute Exacerbation of Chronic Pulmonary Obstrutive Disase

Diagnosis nomenclature
Primary Standard of Present mMRC grading Presence of
Diagnosis diagnosis condition right heart
failure
COPD (GOLD grading ) Stable Grade 0 to 4 Corpulmonale
or AE or no signs of
(Clinical) RHF
e.g 1: COPD (Clinical), AE, mMRC grade 2, with no signs of RHF + other underlying conditions
e.g 2: COPD (Gold II), AE, mMRC grade 2, with cor pulmonale + other underlying conditions
Diagnosis, Initial Assessment and Investigations

Acute change in the following symptom that is beyond day to day variation.
• Dyspnea
• Cough
• Sputum production
Signs of severity
• Use of accessory respiratory muscle
• Paradoxical chest wall movement
• Worsening or new onset of central cyanosis
• Development of peripheral oedema
• Hemodynamic instability
• Detoriation of mental status
mMRC grading of Shortness of breath
• Grade 0: Get breathless with strenuous exercise.
• Grade 1: Short of breath when hurrying on the level or walking up a slight hill.
• Grade 2: Walks slower than people of same age on level ground.
• Grade 3: Stops after walking 100 meters
• Grade 4: Breathless on dressing or undressing
Investigations
• For all patient: Chest X ray and ECG
• For selected patient if indicated (after evaluation): Complete Blood Count, Na, K, Creatinine, RBS,
Urine Routine
Management
Management of Severe but not life threatening exacerbations
• Assessment: ABC, severity of symptoms, blood gas and chest radiograph
• Supplement oxygen:
o Should be titrated to improve patient hypoxaemia with target of saturation of 88-92%
o Arterial blood gas should be checked after 60 minutes to ensure satisfactory oxygenation
without CO2 retention.
• Bronchodilators: SABA+SAAC (Use spacers preferably or nebulizers)

• Corticosteroid: Predinisolone 30-40 mg orally or IV hydrocortisone if patient is unable to swallow

• Antibiotics:
o To be started only for moderately to severely ill patient with increase in cough and sputum
purulence
o Choice of antibiotics: Aminopenicillin with or without clavulanic acid, Macrolids
o Rout of antibiotics: Orally unless patient very sick or cannot take orally
• Noninvasive mechanical ventilation (Please see procedure section for ED-NIV operation): To be
started if at least one of the following is present
o Respiratory Acidosis: (arterial pH ≤ 7.35 and/or PaCO2 ≥ 45mm Hg)
o Severe dyspnea with clinical sign suggestive of respiratory muscle fatigue, increase work of
breathing or both, such as use of use of respiratory accessory muscle, paradoxical motion of
the abdomen, or retraction of the intercostal space.
o
• Invasive mechanical ventilation (Please see procedure section for ED-Ventilator operation)
o Unable to tolerate NIV or NIV failure
o Respiratory or cardiac arrest
o Respiratory pause or loss of consciousness or gasping for air
o Diminished consciousness, psychomotor agitation, inadequately controlled by sedation
o Massive aspiration
o Persistent inability to remove respiratory secretions
o Heart rate < 50 per minute with loss of alertness
o Severe hemodynamic instability without response to fluid and vasoactive drugs
o Severe ventricular arrhythmia
o Life threatening hypoxaemia in patient unable to tolerate NIV
• At all time
o Monitor fluid balance
o Consider subcutaneous heparin or LMWH (If needed)
o Identify associated conditions (Heart failure, arrhythmia)
o Closely monitor condition of patient.
Disposition
Discharge criteria
• Able to use long acting bronchodilators with inhaled corticosteroids
• Inhaled SABA is required no frequently than 4 hours
• Patient if previously ambulatory, is able to walk across the room
• Patient is able to eat and sleep without frequent awakening by dyspnea
• Patient has been clinically stable for 12 to 24 hours
• Arterial blood gas have been stable for 12 to 24 hours
• Patient fully understands correct use of medications
• Follow up and home care management have been completed
• Patient and family are confident that patient can be managed successfully at home
On discharge
• Medication to be adjusted as per guidelines of management of Stable COPD

• Follow up to be arranged in 4 to 6 weeks if stable

• Echocardiogram and PFT to be planned on follow up
Hospital admission criteria

• Marked increase in intensity of symptom such as sudden development of resting dyspnea
• Severe underlying COPD
• Onset of new physical signs (Cyanosis, peripheral oedema)
• Failure of exacerbation to respond to initial medical management
• Presence of serious comorbidities (Heart failure, newly occurring arrhythmia)
• Frequent exacerbations (More than 2 in a year)
• Older age
• Insufficient home support
Indications of ICU admission

• Severe dyspnea that responds to initial emergency therapy
• Changes in mental status (confusion, lethargy, coma)
• Persistent or worsening hypoxaemia (PaO2 < 40 mmHg) and/or severe/worsening respiratory
acidosis (pH < 7.25) despite supplemental oxygen and noninvasive ventilation.
• Need for invasive mechanical ventilation
• Hemodynamic instability – need for vasopressor

Exacerbation
Mild Moderate or severe

Only 1 of 3 cardinal symptoms At least 2 of 3 cardinal symptoms
Increase Dyspnea Increase Dyspnea
Increase sputum volume Increase sputum volume
Increase sputum purulence Increase sputum purulence
Azithromycin
Cephalosporin Risk factors
Doxycycline Uncomplicated COPD • Age > 65 years
Trimethroprim/Sulfamethoxazole No risk factors • FEV1 < 50%
If recent (< 3 months) antibiotic • ≥ 3 exacerbations/ year
exposure, use alternative class • Cardiac cause
Complicated COPD
1 or more risk factors
Is there risk for Pseudomonas?

• Recent hospitalization (2 days'
duration during the past 90 days)
• Frequent administration of antibiotics
Levofloxacin 750mg PO or IV once daily or No (≥4 courses within the past year)
Ceftriaxome IV or • Severe COPD (FEV1 <50 percent of
Cefotaxime IV predicted)
Discharge on Oral
Amoxycilline if stable • Isolation of P. aeruginosa during a
previous exacerbation
• Systemic glucocorticoid use
Yes
Obtain sputum gram stain and

culture and give
Levofloxacin 750mg PO or IV
once daily

Stable Chronic Obstrutive Pulmonary Disease

Diagnosis nomenclature
Primary Standard of Present mMRC grading Presence of
Diagnosis diagnosis condition right heart
failure
COPD (GOLD grading ) Stable Grade 0 to 4 Corpulmonale
or AE or no signs of
(Clinical) RHF
e.g 1: COPD (Clinical), Stable, mMRC grade 2, with no signs of RHF + Other underlying conditions
e.g 2: COPD (Gold II), AE, mMRC grade 2, with cor pulmonale + Other underlying conditions
Diagnosis
History
Dyspnea that is
• Progressive (worsens over time)
• Characteristically worse with exercise
• Persistent
Chronic cough: May be intermittent and may be unproductive
Chronic sputum production: Any pattern of chronic sputum production may indicate COPD.
History of exposure to risk factor
• Tobacco smoke
• Smoke from home cooking or heating fuels
• Occupational dust or chemicals
Family history of COPD
Clinical Findings
Physical signs of airflow limitation are not present unless significant impairment of lung function test has
occurred. Their detection has relatively low sensitivity and specificity. Their absence does not exclude the
diagnosis.
mMRC grading of Shortness of breath

• Grade 0: Get breathless with strenuous exercise.
• Grade 1: Short of breath when hurrying on the level or walking up a slight hill.
• Grade 2: Walks slower than people of same age on level ground.
• Grade 3: Stops after walking 100 meters
• Grade 4: Breathless on dressing or undressing
Pulmonary function test

• Gold 1: Mild – FEV1 ≥ 80% of
• Gold 2: Moderate - FEV1 ≥ 50% - 80%
• Gold 3: Severe - FEV1 ≥ 30% - 50%
• Gold 4: Very Severe - FEV1 < 30%

Management
Non Pharmacological Therapy
• Smoking cessation – For all patient
• Physical activity – For all patient
• Pulmonary rehabilitation – For patient group B – D
• Vaccination (Flu and Pneumococcal): For all patient depending on local policies, availability and
affordability.
Pharmacological Therapy
Patient Group Recommended Alternative choice Other possible

first choice treatment
Group A: SAAC or SABA LAAC or LABA Theophylline
Gold 1 or 2 prn or SAAC + SABA
and/or
Exacerbation per year 0-
1
and
mMRC grading = 0-1
Group B: LAAC or LABA LAAC + LABA SABA and/or

Gold 1 or 2 SAAC
and/or Theophylline
Exacerbation per year 0-1
and
mMRC grading ≥ 2
Group C: ICS + LABA or LAAC + LABA or SABA and/or
Gold 3 or 4 LAAC LAAC + SAAC
and Phosphodiesterase-4 Theophylline
exacerbation per year ≥ 2 inhibitor
and LABA +
mMRC grading 0-1 Phosphodiesterase-4
inhibitor
Group D: ICS + LABA ICS + LABA + LAAC Carbocysteine
Gold 3 or 4 and/or LAAC ICS + LABA +
and Phosphodiesterase-4 SABA and/or
exacerbation per year ≥ 2 inhibitor SAAC
and ICS + LAAA + Theophylline
mMRC grading ≥ 2 Phosphodiesterase-4
inhibitor
*LAAC: Long acting anti cholinergic, LABA: Long acting beta agonist, SAAC: Short acting anti cholinergic,
SABA: Short acting beta agonist

Long term Oxygen Therapy

• Required for following patients
• SaO2 below 88%
• Evidence of pulmonary hypertension
• Peripheral oedema suggesting cardiac failure
• HCT > 55%
Investigations (Requirement to be decided by treating doctor)

Chest X ray, ECG, HCT and Echocardiography
Follow up
Date and day should be specified.
Following areas to be explored on each follow up
• Are you better? (in terms of SOB, work, sleep)
• Is that change worthwhile to you?
• Smoking status
• Device technique

Bronchial Asthma
Introduction
Bronchial asthma is a chronic inflammatory disorder of the airways associated with airway hyper
responsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness and coughing
particularly at night or in the early morning. These episodes are usually associated with widespread but
variable airflow obstruction that is often reversible either spontaneously or with treatment.
Clinical features
• Shortness of breath
• Wheeze
• Cyanosis
• Chest tightness
• Signs of severity:
Respiratory rate ≥ 25/min
Heart rate ≥ 110/min,
Inability to complete sentence in one breath
• Life threatening signs:
Silent chest
Poor respiratory effort
Arrhythmia, exhaustion
Altered conscious level
Asthma COPD
Onset Anytime Mid to late adult life
Smoking ± ++
Cough and Smoking Less common Common
Dyspnoea and exertion Variable Progressive
Nocturnal symptoms Common Uncommon
Airway obstruction Diurnal variation Little variation
Response to CS Good 15-20%
Investigations
• Chest X ray: Exclude pneumothorax and to diagnose any parenchymal infection
• ECG: Usually normal, in severe asthmatics, sign of right heart strain may be present
• Complete blood count: to assess the sign of infection
• Electrolytes: Potassium may be lowered by high dose of beta agonist
Management
1. Secure ABC
2. Sit the patient upright in bed
3. Oxygen: High flow > 10lts per minutes by mask
4. Intravenous access
5. Blood for investigations
6. Nebulisation (Salbutamol 1ml + Ipratropium 1ml + Normal saline 1 ml) repeat 3 times

7. Steroids: Hydrocortisone 200mg iv

8. Antibiotics should be given if there is evidence of infection
Management of bronchial asthma

1st Hour Oxygen Administration if SpO2 is less than 90%, otherwise leave on air.
Inhaled Salbutamol + Ipratropium one nebulisation every 15 minutes for one hour
Oral prednisolone 40-60 mg (1-2mg/kg/day in children)
In patients who can’t tolerate oral meds, give IV hydrocortisone 200mg 6 hourly
2nd Hour Four more doses of inhaled salbutamol and ipratropium
Terbutaline sc 0.3-0.5mg (0.01mg/kg for child) (only if not able to tolerate

nebulizers or not responding to nebulizers)
IV Aminophylline 6mg/kg over 20-30 mins as loading dose (not required if on

deriphylline) and maintenance dose 0.4 to 0.7 mg/kg/hr (* to be used with caution)
IV Magnesium sulphate 2gm over 20 mins

Patient with signs of severity or life threatening signs should be admitted, others can be discharged if they
are stable.
Discharge medication
• Oral steroid 1-3 week
• Inhaled corticosteroid at high dose 1000-1500µgm
• Inhaled long acting beta agonist (salmetrol)
• Oral theophyllines if required
Admission criteria
• Persistent respiratory distress
• Patient without subjective improvement
• Patients with continued wheeze and diminished air movement
• Recent and multiple ED visit
• Symptoms for more than 1 week
• Pneumothorax
• Pneumomediastinum
• Pneumonia
• Fatigue
Discharge criteria
• Patient reports subjective improvement
• Clear lungs with good air movement

Community Acquired Pneumonia
Introduction
Community-acquired pneumonia is defined as an acute infection of the pulmonary parenchyma in a
patient who has acquired the infection in the community
Clinical Features
• Cough with sputum production
• Fever with chills
• Shortness of breath
• Pleuritic chest pain
• Abnormal vital signs: Tachycardia, tachypnoea, hypoxia
• Pulmonary examination: dullness on percussion, increased vocal fremtius, crepitation, ronchi
Prognostic variables: CRB65 (A simplified version of CURB65)

• Confusion (based upon a specific mental test or disorientation to person, place, or time)
• Respiratory rate >30 breaths/minute
• Blood pressure (systolic <90 mmHg or diastolic <60 mmHg)
• Age >65 years
CRB65 score of 0 can be discharged; however score of 1 or more needs admission except for age.
Investigations
1. Complete blood count: Very high count or very low count predicts increased morbidity.
2. Electrolytes, blood sugar and creatinine
3. Sputum for gram stain and culture
4. Blood culture
5. Chest x ray
Management
1. Check ABC
2. Sit the patient upright in bed
3. Check oxygen saturation and bedside blood sugar (if needed)
4. Give oxygen
5. Secure intravenous access
6. Send blood for investigations
7. Pain relief with paracetamol or NSAIDs
8. Empirical antibiotics therapy should be given through oral route in low and moderate severity CAP
admitted to hospital unless there are no contraindications to oral therapy.

CAP
Low severity Moderate severity High severity

CRB65 = 0 CRB65 = Up to 2 CRB65 > 2
Discharge Admission Admission (Consider

critical care)
Preferred Treatment Preferred Treatment
Amoxyciline 500mg three Amoxycilline 500mg t 1 gm Preferred Treatment
times a day for 7 days three times a day plus Co amoxiclav 1.2gms IV three
clarithromycin 500mg twice times a day plus
Alternative Treatment a day for 5 days or unless Clarithromycin 500 mg IV two
Doxycycline 200mg afebrile for 24 hours times a day for 5 days or
loading dose then 100mg If oral administration not unless afebrile for 24 hours
once daily for 5 days or possible : If legionella is suspected add
unless afebrile for 24 Benzyl penicillin 1.2 gms IV levofloxacin
hours four times a day plus
or Clarithromycin 500mg IV If oral administration not
Clarithromycin 500 mg two times a day for 5 days or possible Benzyl penicillin 1.2
twice a day for 5 days or unless afebrile for 24 hours gms IV four times a day plus
unless afebrile for 24 Clarithromycin 500mg IV two
hours times a day
Alternative Treatment
Doxycycline 200 mg loading Alternative Treatment
dose then 100 mg orally or Benzylpenicillline 1.2 gm IV
levofloxacin 500 mg orally four times a day plus
once daily for 5 days or Levofloxacin 500 mg IV two
unless afebrile for 24 hours times a day or Ciprofloxacin
400mg IV two times a day
Or
Ceftriaxone 2gm IV once daily
or Cefotaxime 1 gm IV three
times daily plus
Clarithromycin 500mg IV
twice daily
If Legionella is strongly
suspected consider adding
Levofloxacin

Pneumothorax
Small pneumothorax: visible rim on chest x ray < 2 cm
Large pneumothorax: visible rim on chest x ray > 2 cm
Causes
• Primary Spontaneous: Healthy subjects with no underlying lung disease. More common in young,
smoking men aged 20-40 years.
• Secondary Spontaneous: Pleural rupture due to underlying lung disease.
• Infection: Cavitating pneumonia, TB
• Trauma: RTA
• Iatrogenic: After pleural biopsy or aspiration
Clinical features
• Sudden onset of breathlessness
• Chest pain: Dull, central, heavy
• Signs of significant pneumothorax (Tension pneumothorax)
a. Trachea shift to opposite side
b. Raised JVP
c. Hypotension
d. Tachycardia
e. Shock
Investigation
• Chest X ray
Management
1. Check ABC
2. Keep in upright position
3. Check oxygen saturation
4. Give oxygen
5. Secure intravenous access
6. Aspiration
7. Intercostal drain

Management
Pneumothorax
Primary Secondary
Breathlessness Breathlessness and

and/or rim of air No age > 50 years and/or
No
> 2cm in CXR Aspiration rim of air > 2cm in CXR
Yes Yes
Successful Not Successful
Aspiration Intercostal drain
Successfu
Not Successful Not Successful
Admit for 24 hour
Consider repeat Successful observation Refer to thoracic
Successful surgeon
aspiration
Not Successful
Successful
Intercostal drain
Not Successful
Refer to thoracic
Discharge
surgeon

AMS/HAPE/HACE
The diagnosis of Altitude Sickness
Document the altitude where problem started, document itinerary and rate of ascent, pre existing and co
sxisting illness, past medical history, medication history etc.
Diagnostic criteria for AMS (Acute Mountain Sickness) in a person who recently arrived at high altitude
(2700 and more), the presence of headache and at least one of the following: nausea or vomiting, fatigue
or weakness, dizziness and insomania.
High altitude pulmonary edema (HAPE) is diagnosed if at least 2 of these symptoms and 2 of these signs
are present.
Symptoms: Cough, fatigue, shortness of breath at rest and tightness in the chest
Signs: Crackles in the lung, cyanosis, tachycardia(>120), tachypnea (>20). Patient with HAPE may have no
headache.
High altitude cerebral edema (HACE): This is the end stage of AMS.
Definition: Neurological deterioration in a person with AMS or HAPE, characterized by ataxia and or mental
status changes. If possible on the tandem gait test.
Severely ill people with altitude sickness may have both HAPE and HACE.
Kep in mind other illness lile MI, PE, SAH, CVA, hyponatraemia, diabetes. Just because someone is brought
from the mountains does not mean they have altitude sickens.
Lab test: ECG, Oxygen saturation, Chest X ray, CBC, Urine, Electrolytes, Creatinine, Blood culture if febrile,
malaria smear if relevant, sputum for AFB(in nepalies), stool test (if diarrhea)
High altitude cerebral edema (HACE)
Goal is to reduce brain volume and ICP and stop leak of blood brain barrier.
Adequate oxygen to raise the saturation > 90%
Dexamethasone 4-8mg initially (depending on severity), then 4 mg 6 hourly PO or IV
Coma care i.e. airway protection, bladder drainage, IV fluids, assisted ventilation as indicated (Caution not
to over hyperventilate. Since the respiratory alkalosis already present and the use of oxygen will markedly
reduce cerebral blood flow, further hyperventilation could result in cerebral ischemia)
Consider fursemide or osmotic diuretics in those critically ill
High altitude pulmonary oedema (HAPE)
Oxygen to get the saturation > 90%

Bed rest
Consider chest infection and use suitable antibiotics if gram stain or culture positive
Nifedipine 20-30 mg extended release BID, watch BP
Coma care if necessary
Stool softner
Salbutamol nebulizer
In an anxious dyspneic patient with stable blood pressure consider morphine 2.5mg PRN.

Treatment of HAPE and HACE

Very often the HAPE and HACE treatment may need to be combined.
Chest X ray opacities clear up in a day or two in HAPE, unlike pneumonia. So, a repeat chest x ray to help
establish diagnosis. Intubation in HAPE or HACE is seldom required unless there is a concomitant illness.
Obviously if someone is comatose the hypotensive with HAPE/HACE, do not give nifedipine, lasix or
morphine. Oxygen and steroids are the mainstay and plan for CT/MRI

Abdominal Emergencies
Contents
Gastritis .......................................................................................................................................................... 100
Causes ........................................................................................................................................................ 100
Clinical features.......................................................................................................................................... 100
Investigations ............................................................................................................................................. 100
Management .............................................................................................................................................. 100
Admission criteria ...................................................................................................................................... 100
Discharge criteria ....................................................................................................................................... 100
Upper GI Bleeding .......................................................................................................................................... 101
Introduction ............................................................................................................................................... 101
Causes ........................................................................................................................................................ 101
Severity criteria .......................................................................................................................................... 101
Investigations ............................................................................................................................................. 102
Management .............................................................................................................................................. 102
Pancreatitis .................................................................................................................................................... 104
Introduction ............................................................................................................................................... 104
Causes ........................................................................................................................................................ 104
Ranson’s Severity Criteria .......................................................................................................................... 104
Investigations ............................................................................................................................................. 105
Management .............................................................................................................................................. 105
Discharge criteria ....................................................................................................................................... 105
Liver Failure .................................................................................................................................................... 106
Introduction ............................................................................................................................................... 106
Causes ........................................................................................................................................................ 106
Investigations ............................................................................................................................................. 107
Management .............................................................................................................................................. 107
Acute cholecystitis ......................................................................................................................................... 108
Introduction ............................................................................................................................................... 108
Diagnostic Criteria ...................................................................................................................................... 108
Investigations ................................................................................................................................................. 108
Management .............................................................................................................................................. 108
Acute Appendicitis ......................................................................................................................................... 109
Introduction ............................................................................................................................................... 109
Appendicitis is a painful swelling and infection of the appendix. ................................................................. 109

Diagnostic criteria ...................................................................................................................................... 109
Investigations ............................................................................................................................................. 109
Management.................................................................................................................................................. 109
Intestinal Obstruction .................................................................................................................................... 110
Introduction ............................................................................................................................................... 110
Cause .............................................................................................................................................................. 110
Pediatric consideration .................................................................................................................................. 110
Investigations: ............................................................................................................................................ 110
Management:............................................................................................................................................. 111
PERFORATED VISCUS ..................................................................................................................................... 112
Introduction ............................................................................................................................................... 112
Causes ........................................................................................................................................................ 112
Investigations ............................................................................................................................................. 112
Management .............................................................................................................................................. 112
Acute Diarrhoea ............................................................................................................................................. 113
Introduction ............................................................................................................................................... 113
Causes ........................................................................................................................................................ 113
Investigations ............................................................................................................................................. 113
Management .............................................................................................................................................. 113
Abdominal Trauma (Blunt/Penetrating) ........................................................................................................ 115
Introduction ............................................................................................................................................... 115
Investigations ............................................................................................................................................. 115
Management .............................................................................................................................................. 115
Testicular Torsion ........................................................................................................................................... 116
Investigations ............................................................................................................................................. 116
Management .............................................................................................................................................. 116
Uretetic Colic.................................................................................................................................................. 117

Overview .................................................................................................................................................... 117

Pathophysiology of Renal Colic .................................................................................................................. 117
Presentation of Renal Colic ........................................................................................................................ 117
Stone Location in Renal Colic ..................................................................................................................... 118
Lab Studies in Renal Colic .......................................................................................................................... 118
Imaging Studies in Renal Colic ................................................................................................................... 118
Management of Renal Colic ....................................................................................................................... 119

Gastritis
Causes
Acute gastritis
Drugs: Aspirin, Steroids, NSAIDS
Stress: Sepsis, burn, trauma
Alcohol
Chronic gastritis: H. pylori infection
Clinical features
• Dyspepsia
• Epigastric pain or discomfort
• Bloating, indigestion, heartburn
• Anorexia, nausea, vomiting
• Hematemesis, Malena, pallor
Investigations
• ECG to rule out ischemic heart disease
• Complete blood count (if signs of blood loss)
• Amylase (if persistent pain)
Management
1. Antacid gel
2. GI cocktails: 30ml of antacids plus 10-20 ml of viscous lidocaine
3. H2 antagonist
Admission criteria
• Evidence of upper GI bleeding
• Uncontrolled pain or vomiting
Discharge criteria
• Symptoms relieved
• Unremarkable physical examination

Upper GI Bleeding
Introduction
Upper gastrointestinal bleeding (or haemorrhage) is that originating from the oesophagus, stomach and
duodenum.
Clinical features
• Hematemesis: Bright red, dark clots, coffee ground
• Malena: Black sticky smelly stool
• Weakness/sweating and palpitation
• Postural dizziness and fainting
• Collapse or shock
Causes
• Peptic Ulcer
• Gastroduodenal erosion
• Oesophagitis
• Varices
• Mallory weiss tear
• Upper GI malignancy
• Vascular malformations
Severity criteria
• Age > 60 years
• Shock (BP < 100mmHg systolic in patients < 60 years or < 120mmHg in patients > 60 years).
Measure postural change in BP in patients who are not shocked and change in HR
• Inappropriate Bradycardia or HR > 120 per minute
• Chronic liver disease, other chronic disease (e.g cadiac, renal, respiratory)
• Bleeding diathesis
• Decreased conscious level
Rockall’s Score
Clinical variable Patients scored
0 1 2 3
Age (years) < 60 years 60-79 >80
Shock No Shock HR > 100 HR > 100
SBP > 100 SBP <100
Co morbidity Nil Cardiac Liver, Renal,
Malignancy
Diagnosis Mallory Weiss All other GI tract malignancy
Stigmata of recent None or dark spot Blood in upper GI
bleed tract, adherent clot,
spurter
Score < 3 = excellent prognosis; Score > 8 = high risk of death

Investigations
• Blood grouping and cross matching
• Amylase
• ECG
Management
1. General management
a. Check ABC
b. Check oxygen saturation
c. Give oxygen
d. Open intravenous line with (16-18 G canula both side) normal saline
Classification of Hypovolaemic shock by blood loss in adult
Class I Class II Class III Class IV
Blood loss < 750 750-1500 1500-2000 >2000
volume (ml)
Blood loss (% of 0-15 15-30 30-40 >40
circulating
blood)
Systolic BP No change Normal Reduced Very Reduced
Diastolic BP No change Raised Reduced Very Reduced/
Unrecordable
Pulse Slight 100-120 120(thready) >120 (very
Tachycardia thready)
Respiratory Rate Normal Normal Raised Raised
(>20/mins) (>20/mins)
Mental State Alert, thirsty Anxious or Anxious, Drowsy,
aggressive aggressive or confused or
drowsy unconscious
Blood transfusion should be considered after loss of 30% of circulating volume
e. Send blood for investigations

f. Catheterization (if needed)
g. NG tube (if needed)
h. Peptic Ulcer bleeding: Inj Pantoprazole 80mg IV bolus followed by continuous infusion of 8
mg/hour
i. Variceal bleeding: Octeotride - 100µgm IV bolus followed by a continuous infusion of 25-50
µgm/h

Upper GI Bleeding
Rockall’s Score < 3 Rockall’s Score > 3
Discharge
Hypovolaemia class I Hypovolaemia > class I
Slow infusion of Normal saline 1lts in

Monitor Normal saline 20-30 minutes
Urine output: Aim for
30ml/hour Hypovolaemia class I
Reassess
Signs of overload:
raised JVP, Hypovolaemia > class I
pulmonary oedema,
peripheral oedema Normal saline 1lts in
20-30 minutes
Hypovolaemia class I
Reassess
Hypovolaemia > class I
Blood transfusion 1 Yes Blood available
unit/hour ±
Dopamine support at No
6-10µgm/kg/min
Normal saline 1lts in
20-30 minutes hour ±
Dopamine support at
6-10µgm/kg/min
ICU/ Urgent Endoscopy

Pancreatitis
Introduction
Inflammation of the pancreas due to activation, interstitial liberation and digestion of the gland by its own
enzymes.
Clinical features
• Abdominal pain: Epigastric or generalized of rapid onset but may occur anywhere (including chest),
dull, constant radiating to back or between the scapulae often relieved by leaning forward.
• Nausea, vomiting ± dehydration ± jaundice
• Peritonitis with epigastric tenderness localized rebound tenderness or generalized abdominal
rigidity.
• Tachycardia and hypotension; shock/collapse and respiratory failure in severe cases
• Very rarely signs of bleeding in pancreatic bed; Grey turner’s sign (echymosis in flanks) or Cullen’s
sign (peri umbilical bruising)
• Hypocalcaemia, tetany
Causes
• Common
• Gall stone, Alcohol
• Uncommon:
• Iatrogenic (Post surgery)
• Trauma
• Infections
• Viral: Mumps, Hepatitis A and B
• Bacterial: Mycoplasm
• Drugs: Thiazides, frusemides, NSAIDs etc
• Hypertriglyceridaemia, Hypercalcaemia, Hypothermia
• Pancreatic carcinoma
Ranson’s Severity Criteria

At presentation During the first 48 hours
Age > 55 years Hematocrite fall > 10%
WBC > 16 x 109/L Urea rise >10mM
Glucose > 10mM (Non diabetic) Serum Calcium < 2.0 mmol/L
LDH > 350 IU Base excess > 4 mmol/L
AST > 250u/L PaO2 ,8kPa
Serum Albumin ,32g/l
Estimated fluid sequestration > 6 lts
Score: <3 = Mortality 3% = Mild pancreatitis; ≥ 3 = 15%; ≥ 6 =40%; >7=100%

Investigations
• Lipase, complete blood count: Raised Hematocrite and Leukocytosis
• Electrolytes and creatinine: Creatinine may rise due to hypovolaemia
• Blood glucose: May be raised
• Liver function test: AST and bilirubin is often elevated especially in gallstone pancreatitis
• Calcium: Hypocalcaemia
• Chest X ray: May show elevated diaphragm, pleural effusion
• Abdominal X ray: May show dilated gas filled loop in region of pancreas
Management
a. Check ABC , oxygen saturation, bed side blood sugar
b. IV open with normal saline (Sometimes may need resuscitation)
c. Send blood for investigations
d. Pain management: Pethidine/Procholrperazine
e. Keep NPO, adequate hydration
f. Antiboitics: Ceftriaxone 1gm IV to prevent secondary infection
Pancreatitis
Ranson’s Score < 3 Ranson’s Score > 3
Conservative Aggressive IV hydration (250 ml hourly for

therapy first 48 hours if cardiac status permits) and
antibiotic, enteral or total parental nutrition
Improvement
No
May need critical Yes
Continue antibiotics for 7-10 days,
enteral or total parental nutrition
Admission criteria
• Acute pancreatitis with significant pain, nausea and vomiting,
• Hemorrhagic or necrotizing pancreatitis
Discharge criteria
• Mild acute pancreatitis without evidence of Biliary tract disease and able to tolerate oral fluids
• Chronic pancreatitis with minimal abdominal pain and able to tolerate oral fluids

Liver Failure
Introduction
Acute: Acute liver failure is a potentially reversible severe liver injury with an onset of hepatic
encephalopathy within 8 weeks or appearance of the first symptoms and in the absence of pre existing
liver disease
Acute on Chronic liver failure: Patient with chronic liver disease presenting with decompentation.
Hepatic encephalopathy (HE) is altered brain function is due to metabolic abnormalities, which occur as a
consequence of liver failure.
Causes
Acute liver failure Acute on chronic liver failure
• Drug induced: Paracetamol, Halothane, • Intercurrent infection: Spontaneous
NSAIDs bacterial peritonitis, Pneumonia, Skin
• Viral Hepatitis infection
• Toxins: Mushrooms • Acute GI hemorrhage
• Malignancy: Malignant infiltration • Additional hepatotoxic insult
• Vascular: Ischemic injury, veno- Alcoholic binge
occlusive diesese Acute viral hepatitis
• Others: HELLP syndrome, autoimmune Hepatotoxic drugs
hepatitis • Drugs: Sedatives/narcotics, Diuretics
• Metabolic derangement
• Hypoglycemia
• Electrolyte disturbances
• Major surgery
• Constipation
Clinical features
1. Encephalopathy
Grade Clinical features

0 Minimal hepatic encephalopathy (previously known as sub clinical hepatic
encephalopathy)
Lack of detectable changes in personality or behavior
Minimal changes in memory, concentration, intellectual function, and coordination
Asterixis is absent
1 Drowsy but coherent, mood change
Altered sleep pattern
Asterixis can be detected
2 Drowsy, confused at times, inappropriate behavior.
Obvious Asterixis
3 Very drowsy and stuparose but rousable; alternatively restless, screaming
4 Comatose, barely rousable

2. Metabolic disturbances: Hypoglycemia, Hypokalaemia, Hyponatraemia are common

3. Cardiovascular abnormalities: Diastolic BP falls as disease progresses.
4. Respiratory failure: Hypoxia common
5. Renal failure: decrease urine output, indicates worse prognosis
6. Bleeding problem: Due to derangement of clotting factors
7. Infection
Investigations
• Complete blood count: To see signs of infection
• Blood glucose: Hypoglycemia
• PT/INR: To see risk of bleeding and prognosis
• Liver function test: Albumin low in acute on chronic liver failure
• ECG/Chest x ray: To see infection
• Electrolytes and creatinine: Hypokalaemia, Hyponatraemia, Deranged renal function
Management
1. Assess ABC
2. Check bed side blood sugar
3. IV access and hemodynamic support with colloid or blood, avoid fluid over load.
4. Send Blood for investigations
5. Prophylactic antibiotics: Inj Cefotaxime 1gm IV stat (Cefotaxime 2 gm iv if SBP)
6. N-Acetylcysteine if paracetamol overdose
7. Vitamin K 10mg IV, may need fresh frozen plasma or platelets transfusion
8. If signs of raised ICP: 100 ml of 20% Inj Mannitol
9. Lactulose 20ml by mouth or NG tube, or rectal enema – 300 ml in 700 ml of NS, to be retained for 30
minutes
Liver failure
Acute Box 1 Acute on Chronic

Prophylactic antibiotics: Inj
Follow Box 1 Cefotaxime 1gm IV stat.
Flowchart 26: Management of Liver failure Encephalopathy Encephalopathy
Vitamin K 10mg IV, may Grade 0-1 Grade > 1
Specific Management need fresh frozen plasma
*All patients should be
e.g. N-Acetylcysteine if admitted
or platelets transfusion
paracetamol overdose Follow Box 1 Follow Box 1
Lactulose 10ml by and consider
mouth or NG tube critical care
If no improvement
If no improvement
consider critical care consider critical care

Acute cholecystitis
Introduction
Acute Cholecystitis is inflammation of gall bladder wall.
Clinical features
• Pain over right upper quadrant: sudden onset of severe pain
• Vomiting
• Fever, Tachycardia, sweating, jaundice
• Murphy’s sign: RUQ tenderness and peritonism especially in inspiration
Acalculous Cholecystitis is seen in elderly or patients with co existing disease or rauma and patients on
total parental nutrition.
Diagnostic Criteria
A Local signs of inflammation
1. Murphy’s sign 2. RUQ mass/pain/tenderness
B Systemic Signs of Inflammation
1. Fever 2. Elevated CRP 3. Elevated WBC count
C Imaging finding characteristics of Cholecystitis
Definitive diagnosis
1. Any one of A and one of B
2. C confirms diagnosis when acute Cholecystitis is suspected clinically
Investigations
• Complete blood count: Increase WBC cout
• Amylase: May be elevated
• USG abdomen: Gall stone, Biliary sludge, thickening of gall bladder wall
Management
1. Assess ABC
2. IV access and NPO
3. Send Blood for investigations
4. Pain management: NSAIDs
5. Admission
6. IV antibiotics: Inj Cefotaxime 1 gm IV stat + Inj Metronidazole 500mg IV stat
*All cases of cholecystitis should be admitted for parenteral antibiotics, analgesia, fluid replacement

Acute Appendicitis
Introduction
Appendicitis is a painful swelling and infection of the appendix.
Clinical features
• Pain abdomen: Occurs suddenly, often causing a person to wake up at night, initially over upper
abdomen then moves lower and to the right, gets worse in a matter of hours, aggravated by
moving, taking deep breaths, coughing, or sneezing
• Other symptoms: Loss of appetite, nausea, vomiting, constipation or diarrhea, inability to pass gas,
a low-grade.
• McBurney’s point tender: Junction between lateral 1/3 and 2/3 of spinoumbilical line at right
• Rovsing’s sign: Pressure on left aggravates pain on right side
• Rebound tenderness
Diagnostic criteria Alvarado Score
Alvarado score (MANTERALS)
• M: Migration of pain to right iliac fossa (1) <5: Appendicitis less likely
• A: Anorexia (1)
• N: Nausea/vomiting (1) 5-6: Possible appendicitis
• T: Tenderness in right iliac fossa (2)
7-8: Probably appendicitis
• R: Rebound tenderness (1)
• E: Elevated temperature (1) >8: Very probably appendicitis
• L: Leukocytosis (2)
• S: Shift to right (1)
Investigations
• Complete blood count: Leukocytosis
• Urine routine examination: To rule out urinary tract infection
• USG pelvis: Especially important in female to rule out other pelvic conditions
Management
1. NPO and IV assess
2. NSAID for pain management
3. Antibiotics: Inj Cefotaxime 1gm/Ciprofloxacin 200mg IV stat + Inj Metronidazole 500mg IV stat (if
planned for surgery single dose prophylactic preferred)
4. Prepare for surgery

Intestinal Obstruction
Introduction
Obstruction of normal flow of intestinal contents due to mechanical or nonmechanical causes.
Cause
• Small Bowel
• Adhesion: Most common
• Hernias
• Neoplasm
• Stricture: Inflammatory bowel disease
• Ascaris
• Large Bowel
• Carcinoma
• Volvulus
• Diverticular disease
• Inflammatory disease
• Ischemic colitis
Pediatric consideration
• Intussusceptions: Most common in 3-12 months of age
• Incarcerated inguinal hernia
• Malrotation with volvulus: Can occur as early as 3-7 days, double bubble often seen in upright
abdominal radiograph due to partial obstruction of duodenum resulting in air in stomach and in
first part of duodenum
• Pyloric stenosis: Onset usually 2-5 weeks of age
Clinical features
• Pain abdomen: Intermittent early, constant with strangulation
• Vomiting: Bile stained emesis with proximal obstruction, feculent emesis with distal obstruction
• Obstipation
• Tachycardia, Hypotension with significant fluid loss
• Fever with strangulation or perforation
• Hyperactive or high pitched bowel sound
• Diffuse abdominal tenderness
• Pain out of proportion to findings suggests ischemic or gangrenous bowel
• Guarding and rebound tenderness
• Hernias: Inguinal, femoral
Investigations:
• Chest X ray erect with both dome of diaphragm: To see gas under diaphragm indicating perforation
• Abdominal X ray erect: To see air fluid level

• Abdominal X ray supine: To see maximum dilatation (normal small bowel < 3 cm in diameter).
Dilatation of cecum > 13 cm indicates potential rupture
• Complete blood count: Leukocytosis
• Electrolytes and Creatinine
• Blood sugar
• Amylase
• Urine routine examination
Management:
1. Secure ABC
2. Normal saline resuscitation when significant volume depletion, strangulation or perforation
3. NG tube suction
4. Foley catheterization
5. Analgesics as needed
6. Antiboitics: Inj Ceftiraxone 1 gm IV stat + Inj Metronidazole 500mg IV stat
7. Liaison with surgical team

PERFORATED VISCUS
Introduction
It is a perforation of any segment of GI tract due to inflammation, ulceration, trauma or obstruction.
Chemical peritonitis occurs as a result of spillage of gastric or intestinal contents into peritoneal cavity.
Causes
• Peptic ulcer disease
• Appendicitis
• Enteric fever
• Inflammatory bowel disease
• Diverticular disease
• Colon carcinoma
• Foreign body ingestion
• Trauma
Clinical features
• Sudden and severe abdominal pain
• Rigidity, Guarding, Rebound tenderness
• Absent bowel sound
• Tachycardia, Hypotension
Investigations
• Chest x ray erect: Gas under diaphragm (pneumoperitoneum).
• Electrolytes, Createnine, blood sugar, Amylase
• ECG
Management
a. ABC
b. Correct hypovolemia: rapid fluid resuscitation with 0.9% NS 1 L in adults and 20ml/kg in children
c. NG tube, Catheterization
d. Broad spectrum antibiotics: Inj Ceftriaxone 1 gm iv stat + Inj Metronidazole 500 mg iv stat

Acute Diarrhoea
Introduction
Diarrhea reflects increased water content of the stool, whether due to impaired water absorption and/or
active water secretion by the bowel. In severe infectious diarrhea, the number of stools may reach 20 or
more per day, with defecation occurring every 20 or 30 minutes.
Causes
Pathogen Small bowel Colon
Virus Roravirus Cytomegalovirus
Bacteria Salmonella* Campylobacter*
Escherichia coli* Shigella
Clostridium perfringens Clostridium difficile
Staphylococcus aureus Yersinia
Aeromonas hydrophila Vibrio parahaemolyticus
Bacillus cereus Enteroinvasive E. coli
Vibrio cholerae Plesiomonas shigelloides
Klebsiella oxytoca(rare)
Protozoa Cryptosporidium* Entamoeba histolytica
Cyclospora
Giardia lamblia
Clinical features
• Pulse rate > 90
• Postural hypotension
• Supine hypotension and absence of palpable pulse
• Dry tongue , Sunken eyeballs, Skin pinch
• Signs of severity:
• Disorientation, lethargic
• Anuria
• Hypotention, cold perphhery
Investigations
• Stool routine examination: Fecal leukocyte > 10/hpf is an indicator if invasive diarrhea requiring
antibiotics
• Stool for hanging drop: For cholera
• Electrolytes and creatinine: In case of severe dehydration
Management
1. ABC, Check vitals, Check blood sugar
2. IV lock and send blood for investigation if needed
3. Catheterization (if in shock)
4. ORS or IV fluid as per need

Acute Diarrhoea
Dysentry: Mucoid, blood mixed Watery Diarrhoea
Emperical Antibiotics:
Cholera
Ciprofloxacin 500mg twice a Rice watery stool,
day for 3 days excessive volume
loss with hanging
If resistant to ciprofloxacin or drop positive
camphylobacter infection Not Suggestive of
Cholera
Azithromycin 500mg daily for 3
Aggressive fluid
days
management
Doxycycline
300mg stat or
Azithromycin 1gm
stat
Hemodynamically unstable
Hemodynamically stable
IV fluid bolus at least 2 liters or NS
or RL + Antiboitics (Ceftriaxone)
ORS as tolerated
IV fluid: Maintenance
Stable 100/50/20 rule
Reassess
Or bolus if required Discharge if
Unstable
improvement
Fluids + Ionotropic
support

Abdominal Trauma (Blunt/Penetrating)
Introduction
• Injury results from a sudden increase of pressure to abdomen.
• Solid organ injury usually manifests itself as hemorrhage
• Hollow viscous injuries result in bleeding and peritonitis from contamination with bowel contents.
• Solid organ injury is more frequently than hollow viscous
• Spleen is the most frequently injured organ followed by liver, intestine, retroperitoneal structures
and kidney
• In penetrating injury liver is most commonly injured followed by small bowel,stomach, colon, major
vessel and less often the spleen
Clinical features
• Pain abdomen
• Nausea and vomiting
• Labored respiration due to diaphragm irritation of upper abdominal injury
• Left shoulder pain with inspiration from diaphragmatic irritation due to bleeding
• Signs of peritonitis: Abdominal guarding, rebound tenderness
• In severe intra abdominal bleeding: Pallor and Shock
Investigations
• Hematocrite
• Blood grouping and cross matching
• Urine Routine examination
• X ray abdomen erect (if patient is hemodynamically stable)
• USG abdomen (if unstable, doctor should accompany)
• Four quadrant aspiration
Management
• C spine stabilization if needed
• A: Check airway and give oxygen
• B: Examine chest
• C: Two large bore IV with crystalloid infusion
• Apply sterile dressing to open wound
• Prepare for blood transfusion if needed
• Foleys catheter if patient is in shock
• NG tube if there is features of peritonitis
• Tetanus toxoid in penetrating injury
• Inj Ceftriaxone + Inj Metronidazole if penetrating injury
• Pain management: Opioids analgesics

Testicular Torsion
Testicular torsion is a true urologic emergency and must be differentiated from other complaints of
testicular pain because a delay in diagnosis and management can lead to loss of the testicle. Though
testicular torsion can occur at any age, including the prenatal and perinatal periods, it most commonly
occurs in adolescent males; it is the most frequent cause of testicle loss in that population
History includes a sudden onset of severe unilateral scrotal pain.

• Scrotal swelling
• Nausea and vomiting
• Fever (16%)
• Urinary frequency (4%)
Investigations
• Urinalysis
• Complete blood count: CBC can be normal or show an elevated WBC count in as many as 60% of
patients who have torsion.
Management
• Early diagnosis and prompt urologic consultation is essential since time is critical in salvage of the
testicle.
• Analgesic pain relief should be administered as testicular torsion is typically very painful.
• Attempt manual detorsion with pain relief as the guide for successful detorsion. The procedure is
similar to the "opening of a book" when the physician is standing at the patient's feet.
• Surgical management
• Most torsions twist inward and toward the midline; thus, manual detorsion of the testicle involves
twisting outward and laterally.
• The physician then rotates the right testicle outward 180° in a medial to lateral direction.
• Rotation of the testicle may need to be repeated 2-3 times for complete detorsion and to provide

Uretetic Colic
Overview
1. In the US, renal colic affects 5% of the population.
a. The incidence is lower in non-industrialized countries.
b. The male-to-female ratio is 3:1
c. Peak age of onset is 20-40 years.
2. Beware of a "first episode of renal colic" in a patient >60 years old (ie. consider AAA)
a. Nephrolithiasis in children is rare.
3. Without preventative treatment, recurrence rates after the first kidney stone are:
a. 15% by 1 year
b. 35% by 5 years
c. 50% by 10 years
Pathophysiology of Renal Colic

1. Most renal calculi are formed in the kidney when the urine becomes supersaturated with a salt
capable of forming crystals.
a. These crystals are then flushed into the ureter
2. Rates of spontaneous stone passage are determined by:
a. Stone size (#1), Stone location
3. The "classically-described" critical stone size is 4mm.
4. According to this "classic" teaching:
a. Stones <4mm have a 90% rate of spontaneous passage within 4 weeks (especially if located
in the lower ureter).
b. Stones 5-8mm have only a 15% rate of spontaneous passage.
c. Stones >9mm have only a 5% rate of spontaneous passage.
5. Since most stones are small, the overall spontaneous passage rate is 85%.
6. Since 2010, however, larger and larger stones are being considered for trials of conservative
management.
7. Risk factors for renal colic include:
a. Hypercalcemia
b. Sarcoid
c. Crohns
d. Renal Tubual Acidosis (Type 1)
e. Recurrent UTI
Presentation of Renal Colic

1. The pain in renal colic is caused by:
2. Ureteral obstruction and spasm
3. +/- Associated infection
a. There is no correlation between degree of pain and likelihood of obstruction.
b. The "classic" renal colic patient presents:
4. Squirming with pain
5. Unable to lie or sit still

6. Fever is not part of uncomplicated renal colic, and suggests infection.
Stone Location in Renal Colic

1. There are five narrowings in the urinary tract where stones typically impact:
a. Renal calyx
b. Ureteropelvic junction (UPJ)
c. Pelvic brim (where the ureters arch over the iliac vessels)
d. Ureterovesical junction (UVJ) (ie. the narrowest part of the ureter)
e. Bladder neck
2. The location of pain may suggest the position of the impacted stone:
3. Calyx or UPJ stones often present with flank pain (ie. distension of the renal capsule).
4. Ureteral stones can cause abrupt, severe, colicky pain in the flank and lower abdomen
5. UVJ stones can cause irritative voiding symptoms (eg. urinary frequency and dysuria)
6. Bladder stones are usually asymptomatic
7. Persistent bladder stones typically arose in the bladder--not in the kidney or ureter. They are
different entities than kidney stones
Lab Studies in Renal Colic

1. Urinary RBCs
a. Most patients with renal colic have some degree of hematuria
b. The degree of hematuria is not predictive of stone size or likelihood of passage.
2. Urinary WBCs
a. Pyuria (ie. >5 WBC/hpf on a centrifuged specimen) is sensitive, but not specific, for
associated infection
3. Serum Cr
a. Even if unilateral, large obstructing stones can cause a temporary rise in creatinine.
Imaging Studies in Renal Colic

1. Most authors recommend diagnostic imaging:
a. For first-time stones
b. If the diagnosis is unclear
c. If suspected proximal infection (ie. to rule out an obstructing stone)
2. KUB (kidney-ureter-bladder) X-ray
a. Sensitivity is <70-90% for renal stones
b. Specificity is low
3. Renal U/S
a. Findings suggesting renal colic on U/S include:
b. Direct visualization of the stone (uncommon)
c. Hydroureter >6 mm or hydronephrosis (with obstructing stones)
4. Advantages of U/S include the lack of radiation.
5. CT scan
6. Advantages of CT for renal colic include:
a. Specificity and sensitivity both >95-100%
b. Rapid study (<5 mins)

c. No contrast
d. Can determine the size of the stones
e. Can diagnose other pathologies causing pain (eg. AAA, ovarian disorders)
Management of Renal Colic

1. IV fluids
a. This is controversial.
b. Some sources believe that IV fluids hasten passage of the stone
c. Other sources believe that the increased hydrostatic pressure only exacerbates pain
2. NSAIDs
a. NSAIDs are a first-line agent in renal colic.
b. Ureteral obstruction stimulates prostaglandin synthesis in the renal medulla--which
increases ureteral contractility.
c. NSAIDS inhibit prostaglandin synthesis
d. Disadvantages of NSAIDs include a lag-time of 15-30 minutes before efficacy.
e. However, after this time, they are at least as effective as opioids in this setting
f. Obviously, both NSAIDs and opioids can (and generally should) be given simultaneously
3. Opioids
a. Advantages of opioids for renal colic include:
b. Rapid-onset
c. Inexpensive
4. Antiemetics
5. +/- Tamsulosin ("Flomax")
a. This is commonly used to promote stone passage.
b. However, the literature regarding the benefit of this therapy is conflicting
c. If used, one reasonable dosing regimen is 0.4mg PO qd for 2 weeks
6. +/- Foley catheteriziation
a. This may be useful for patients with an obstructing bladder-neck stone.
7. +/- Antibiotics (if evidence of associated infection)
a. Signs of infection might include:
1. Fever
2. +/- Elevated WBC (but this could also be a simple response to pain)
3. +/- Positive U/A (sensitive, but non-specific)
b. Infected hydronephrosis in the setting of an obstructing stone is the most dangerous
presentation of renal colic--and requires urgent:
4. Broad-spectrum antibiotics
5. Urology consultation for a drainage or removal procedure
8. Also consider Urology consultation for renal stones associated with:
a. Solitary kidney
b. Kidney transplants
c. AKI
d. Stone size >4mm (although this is highly variable)
e. Intractable pain
f. Inability to tolerate oral fluids or medications

Neurological Emergencies
Contents
Headache ....................................................................................................................................................... 120
Meningitis ...................................................................................................................................................... 121
Investigations ............................................................................................................................................. 121
Management .............................................................................................................................................. 121
Seizure ............................................................................................................................................................ 122
Seizure Physiology...................................................................................................................................... 122
Status Epilepticus ....................................................................................................................................... 122
Pathophysiology of Status Epilepticus ....................................................................................................... 122
Management of an Actively-Seizing Patient .............................................................................................. 123
Empiric therapy for drug-induced seizures................................................................................................ 125
Cerebrovascular Accident (CVA) .................................................................................................................... 127
Introduction ............................................................................................................................................... 127
Investigations ............................................................................................................................................. 127
Management .............................................................................................................................................. 127
Head Injury ..................................................................................................................................................... 128
Introduction ............................................................................................................................................... 128
Clinical feature ........................................................................................................................................... 128
Investigation............................................................................................................................................... 128
Management .............................................................................................................................................. 129
Referral Criteria.......................................................................................................................................... 129
Discharge Criteria ....................................................................................................................................... 129
Treatment of raised ICP ................................................................................................................................. 130
Headache
Headache
Occurs more than 15 days per Yes

month for more than 3 months Chronic Headache
No Secondary
Primary Those associated
New onset headache or headache
Those not associated with underlying
different form their usual headache Yes
with underlying No pathology:
OR
pathology: Infection,
With danger signs*
Migraine, tension, neoplastic,
cluster headache vascular or drug
induced
Cluster Inj Sumatriptan

Bilateral Unilateral Headache 6mg subcutaneous
is recommended
No
Tension With following features
Infection: Yes Fever
Headache Duration: 4-72 hours
Meningitis
Onset: Gradual
Brain Abscess No
Frequency: 1-2/month
Aspirin or Restlessness during Neurological
Paracetamol attack: 0% Yes
CVA Signs
Ipsilateral autonomic
feature: Occasionally Neoplastic No
Yes Associated with
Refer to Section on CVA drug: Present for
Migraine and Meningitis for 15 days or more
per month
increased on
Management taking medicine:
• Opoids analgesic should not be routinely use
• Paracetamol 1gm PO for mild to moderate migraines
• Aspirin 900mg or Ibuprofen 400mg PO for severe migraine
Can be managed on
• If not improving or if previous attacks have not been
OPD basis once
controlled by simple analgesics, oral triptans (Amlotriptan
acute pain decreases
12.5, Eletripran 40-80 mg or Riaztriptan 10 mg) are
recommended
• If not controlled add oral Naproxen 500mg
• Oral Metoclopramide to decrease nausea and vomiting

Meningitis
Clinical features
• Classical triad: Fever, Neck rigidity, and a change in mental status
• Headache
• Older adults (especially those with underlying conditions such as diabetes mellitus or
cardiopulmonary disease) may present insidiously with lethargy or obtundation, no fever, and
variable signs of meningeal inflammation
• Seizures, focal neurologic deficits
• Skin manifestations: Petechiae and palpable Purpura(N. meningitidis)
• Brudzinski's sign: Spontaneous flexion of the hips during attempted passive flexion of the neck
• The Kernig's sign: Inability or reluctance to allow full extension of the knee when the hip is flexed
90º.
• Accentuation of headache by horizontal rotation of the head at a frequency of two to three times
per second
Investigations
• CSF analysis: LP should be done unless contraindicated
Total WBC count Protein (gm/L) Glucose (mg/dl)
Viral Meningitis 5-100 0.5-2.5 Normal
Bacterial Meningitis > 1000 > 2.5 10-45
Tubercular Meningitis 100-1000 > 2.5 10
• Complete blood count, blood culture, electrolytes and creatinine, blood glucose
• ECG and Chest X ray
Management
1. Secure ABC, oxygen, keep vein open with Normal saline, send blood for investigations
2. Check bedside blood sugar, Catheterization (if needed)
3. IV steroids: Dexamethasone 0.15-0.4 mg/kg every six hours for four days (must be started before or
with Abs and main use is in pneumococcal and in non HIV)
Recommendation for empirical therapy
Age Common Bacterial Pathogen Antibiotics
< 1 month Streptococcus agalactiae, Escherichia Ampicillin plus cefotaxime; OR
coli, Listeria monocytogenes, ampicillin plus an
Klebsiella species aminoglycoside
1-23 months Streptococcus pneumoniae, Neisseria Vancomycin plus a third-
meningitidis, S. agalactiae, generation cephalosporin
Haemophilus influenzae, E. coli
2-55 years N. meningitidis, S. pneumoniae Ceftriaxone 2gm iv stat
>55 years S. pneumoniae, N. meningitidis, L. Certriaxone 2 gm iv stat plus
monocytogenes, aerobic gram- Ampicilline 1gm iv stat
negative bacilli

Seizure
Seizure Physiology
1. The brain is constantly in a state of balance between inhibition (mediated mainly by GABA) and
excitation (mediated mainly by glutamate).
a. Even small shifts in this balance can have dramatic effects
2. GABA is a chemical which binds to the GABA-receptor in the brain.
a. It is activation of the GABA-receptor that inhibits neurotransmission
3. Additional agonists of the GABA-receptor include:
a. BZPs
b. Barbiturates
However, these agonists are not effective unless GABA is also present.
Status Epilepticus
1. Status epilepticus was classically defined as either:
a. A seizure lasting >30mins
b. Multiple seizures cumulatively lasting >30mins without a return to normal LOC
2. Numerous changes for this definition have been proposed (eg. decreasing the time period to 5-10
minutes), but none have been universally accepted.
a. In practice, any seizure lasting >5mins should be treated as status epilepticus
3. Patients with a previously-normal mental status who have a generalized seizure should start to
wake up within 30 minutes.
a. Patients who do not do this may have "non-convulsive status epilepticus" (NCSE)--in which
their body is no longer actively seizing, but their brain continues to seize
b. These requires EEG to detect
Pathophysiology of Status Epilepticus

1. Prolonged seizures reliably damage the brain.
2. Simply controlling the visible seizures does not reduce brain injury or mortality.
a. Brain injury in seizure results from exhaustion of ATP--leading to breakdown of cellular
gradients.
b. This is why paralytics (which stop the body from seizing, but do not stop the brain) are not
effective in status epilepticus. In fact, they are potentially dangerous--as they can mask
ongoing seizures.
3. The most common precipitants of status epilepticus in adults are:
a. Stroke
b. Drugs
c. Ischemia
d. Metabolic abnormalities (eg. hypoglycemia, hyponatremia)
4. he most common precipitants of status epilepticus in children are:
a. Febrile seizure (#1)
b. Epilepsy
c. Medication change
d. Congenital abnormalities

e. Metabolic abnormalities (eg. hypoglycemia, hyponatremia)
Management of an Actively-Seizing Patient

Summary
a. Supportive treatment
b. Check glucose
c. Check electrolytes (ie. Na, Ca, Mg)
d. BZPs
e. Phenytoin and/or Phenobarb
f. Propofol (if available)
g. Not generally paralytics (unless required for other indication)
h. +/- Empiric therapy for drug-induced seizures (eg. INH, oral hypoglycemics, TCAs)
i. +/- Empiric therapy for other reversible causes of seizure (eg. eclampsia, intracranial lesion)
j. ICU admission and treatments
Initial Management
1. Supportive treatment
a. Remember that the vast majority of seizures in the ED resolve in <1 minute.
i. Aside from placing the patient in the recovery position, these patients may not need
any other treatment
b. For prolonged seizures, consider need for intubation.
i. Short seizures are not an indication for intubation, but status epilepticus is such an
indication
ii. Avoid Etomidate as an induction drug (as it can lower the seizure threshold)
iii. Always remember that intubation is not a failure of management in status
epilepticus.
1. Instead, intubation is often the natural progression of appropriate
management
2. Status epilepticus is actively harmful to the brain--and the first priority should
be stopping the seizure
3. Never hesitate giving an appropriate medication because you are worried
about potentially having to intubate the patient
c. Consider antibiotics +/- antivirals
d. Since lumbar punctures are potentially contraindicated in recently-seizing patients, consider
the need for empiric treatment for meningitis (or other infections)
2. Check glucose
a. Both hypoglycemia and extreme hyperglycemia can cause seizures.
3. Check electrolytes
a. Check Na, Ca, and Mg
i. An ABG will rapidly tell you the Na and Ca
ii. Regular venous bloodwork is required to check the Mg
b. Seizures can be caused by:
i. Hyponatremia (<110-120mmol/L) or hypernatremia (>160mmol/L)

ii. Hypocalcemia
iii. Severe hypomagnesemia (Mg <0.4mmol/L)
4. BZPs
a. Commonly-used agents (ie. pediatric dose in brackets) in seizure include
i. Diazepam 10mg (0.25mg/kg in peds) IV q1min prn--to an initial max dose of 50-80mg
in adults
ii. Lorazepam 2mg (0.1mg/kg in peds) IV q1min--to an initial max of 8mg in adults
iii. Midazolam 2mg (0.1mg/kg) IV or 4mg (0.2mg/kg) IM--to an initial max dose of 8mg
in adults
b. For seizure control:
i. Onset-of-activity is essentially the same for all of the BZPs above
ii. The duration of activity is longer for Lorazepam than the other two agents
5. Phenytoin
a. The initial dose of Phenytoin is 20mg/kg.
i. The maximum administration rate is 1mg/kg/min (max 50mg/min)
ii. As such, most doses of Phenytoin take >20 minutes to administer (not including
preparation time)
b. Therefore, Phenytoin rarely stops the current seizure.
i. Instead, the main goal with Phenytoin is to prevent subseuqent seizures
c. Following the initial loading dose, a typical maintenance dose is 300mg IV/PO qhs.
d. Remember that Phenytoin has not role (whatsoever) in drug or toxin-induced seizures (ie.
not effective in that setting).
6. Phenobarbital
a. The initial dose of Phenobarb is 20mg/kg.
i. It is administered at a rate of 1mg/kg/min (max 50-75mg/min)
b. Phenobarb may be preferred to Phenytoin in patients aged 1-2 years (and possibly up to 5
years).
i. In this age group, Phenytoin is erratically absorbed
c. Potential side-effects of Phenobarb include:
i. Decreased LOC
ii. Apnea
iii. Hypotension
7. Propofol (if available)
a. In many centres, this agent has replaced Phenobarbital for management of ongoing
seizures.
b. Its mechanism of action includes both GABA-agonism and glutamate-antagonism.
c. Standard doses of Propofol can be used in status epilepticus:
i. Adults -- 50mg bolus(es) followed by an infusion of 0-300mg/hr
ii. Pediatrics -- 1-2mg/kg bolus(es) followed by 1-10mg/kg/hr
d. Most patients will require intubation at these doses.
8. Generally avoid paralytics (unless required for another indication)
a. As mentioned, paralytics stop the outward manifestations of seizure, but do not:
i. Stop the brain from seizing
ii. Fix the underlying etiology

iii. Improve mortality

b. That said, there may be a limited number of indications for giving a paralytic to a seizing
patient:
i. To facilitate intubation
ii. To facilitate imaging studies (eg. CT head)
iii. To facilitate a surgical procedure (eg. cricothyroidotomy, burrhole, etc.)
Empiric therapy for drug-induced seizures

1. For patients who are still seizing despite the measures above, a drug- or toxin-induced etiology
should be considered.
2. Three important drug-induced causes of status epilepticus for which a specific treatment exist
include:
a. INH overdose
b. Oral hypoglycemic overdose
c. TCA overdose
3. Other medications that can potentially cause status epilepticus include:
a. Theophylline
b. Carbon monoxide
c. Buproprion
d. Essentially any medication (other than BZPs)
Seizures from INH overdose

1. Producing GABA in the body requires Pyridoxine (ie. Vit B6)
a. This process is inhibited by INH
2. INH-overdose-induced status epilepticus is characterized by:
a. Persistent seizure activity refractory to all standard treatments
b. A resultant profound lactic acidosis
3. The treatment for INH-induced seizures is gram-for-gram replacement with Pyridoxine.
a. For example, if the patient overdosed on 2g of INH, give 2g of Pyridoxine.
b. More commonly, if the amount of INH overdose is not known, the initial empiric dose of
Pyridoxine is:
i. 5g in adults
ii. 70mg/kg in peds
c. Pyridoxine should be effective within a few minutes.
i. If the Pyridoxine is not rapidly effective (or if the seizures stop but then recur), the
dose of Pyridoxine should be repeated--potentially many times.
ii. Pyridoxine is extremely safe (ie. the maximum safe dose is hundreds of mg/kg)
iii. Unfortunately, in severe INH overdoses, the hospital may run out of Pyridoxine
before the seizure is controlled
iv. In this situation, consider barbiturate coma (which is definitely not ideal, but is the
only other way of possibly stopping the seizure)
Seizures from oral hypoglycemic agent (OHA) overdose

1. OHA overdose with certain agents (eg. sulfonylureas, meglitinides) can cause a refractory
hypoglycemia that leads to status epilepticus.
2. These patients can have refractory hypoglycemia even if kept on a high-dose glucose infusion.
a. The first-line treatment in this case is Octreotide
b. Diazoxide is a second-line treatment if Octreotide is not available
3. Octreotide works in OHA overdose by blocking insulin release from the pancreas.
a. The dose of Octreotide in this setting is 50-100ug SC q6h prn until serum glucose is stable
b. Onset of action is reasonably rapid
c. Stabilization of serum glucose usually takes 24 hours, but may take longer depending on the
type and dose OHA
d. Side-effects of Octreotide are usually minimal.
4. Diazoxide has a similar mechanism of action as Octreotide.
a. However, it is less-effective and has more hemodynamic side-effects (eg. vasodilation and
hypotension)
b. As such, it should only be used in this setting if Octreotide is not available
i. There is no indications for simultaneous use of Octreotide and Diazoxide
5. Glucagon may be useful for patients with ongoing hypoglycemia despite the treatments above.
a. Glucagon works in by recruiting hepatic glycogen and promoting gluconeogenesis.
b. The dose of glucagon in OHA toxicity can be anywhere from 1-10mg/hr (ie. an IV infusion).
c. For patients in whom an IV cannot be obtained, 1mg SC/IM doses can be administered.
i. The time-of-onset with IM dosing is 9 minutes
Seizures from TCA overdose

1. The management of TCA toxicity is a whole talk in itself.
2. In short, initial management of TCA toxicity is with NaHCO3 boluses followed by an infusion.
Consider empiric therapy for other reversible causes of seizure
1. For patients who are still seizing despite the measures above, other reversible etiologies of seizure
should be considered.
2. Two additional causes of status epilepticus for which a specific treatment exist include:
a. Eclampsia -- Give MgSO4 4g IV over 20mins, followed by an infusion of 2g/hr
b. Intracranial lesion -- Get an urgent CT head and consult Neurosurgery as needed
ICU admission and ongoing treatment

For patients with ongoing seizures despite the management steps above, various additional treatments in
the ICU may include:
a. Novel antiepileptics (eg. Keppra, Lamictal)
b. Barbiturate coma
c. Inhaled anesthetics
d. +/- Ketamine infusion

Cerebrovascular Accident (CVA)
Introduction
Cerebrovascular accident is an interruption of the blood to a specific region of the brain. It may be
ischemic or hemorrhagic.
Transient ischemic attack (TIAs): Focal neurological deficit that completely resolve in 24 hours
Risk Factors
• Diabetes, Hypertension
• Smoking
• Coronary artery disease, Peripheral vascular disease
• Oral contraceptive use
Clinical features
• Anterior cerebral artery: Contralateral hemiplegia, Hemisensory loss, apraxia, confusion, impaired
judgment
• Middle cerebral artery: Contra lateral hemiplegia, hemisensory deficits, homonymous hemianopsia,
dysphasia, dyslexia, agnosia
• Posterior cerebral artery: Cortical blindness in half the visual field, visual agnosia, altered mental
status, impaired memory, third nerve palsy
• Vertebrobasilar system: Impaired vision, visual field defects, nystagmus, diplopia, vertigo, dizziness,
facial paresthesia, cranial nerve palsies
• Commences suddenly and peak deficit is established within 24 hours.
• Variable depression of consciousness suggests subdural haematoma.
• Seizure may occur
Investigations
• Electrolytes and creatinine, Blood sugar
• ECG
• Urine R/E
• CT scan
Management
• ABC
• Oxygen, Propped up position
• IV access (avoid 5% dextrose), send blood for investigation
• Check bed side blood sugar
• Aspirin 300mg stat (if CT shows ischemic)
• Treat elevated blood pressure if systolic BP > 220 and diastolic BP > 120 mmHg
• Control seizure with benzodiazepines and Phenytoin
• Treat increased ICP and cerebral oedema (headache, vomiting, Cushings response: Hypertension,
Bradycardia and altered respiratory pattern) with mannitol

Head Injury
Introduction
Primary Head trauma
• Concussion: Head trauma associated with transient loss of consciousness or amnesia with no
evidence of intracranial pathology in CT
• Contusion: Focal injuries to brain characterized by coup (beneath area of contact) or countercoup
(area remote to contact)
• Diffuse axonal injury: Microscopic injuries scattered throughout the brain in a patient in deep coma
Secondary Head trauma
• Epidural Hematoma: Classically transient loss of consciousness with lucid interval. Hematoma will
appear convex in CT.
• Subdural Hematoma: Bleeding into subdural space. Hematoma will appear concave in CT.
• Intracerebral hemorrhage: Bleeding into brain parenchyma.
Clinical feature
• Evidence of head trauma
• Scalp laceration, echymosis
• Raccoon’s eye: bilateral echymosis of orbits
• Battle’s sign: echymosis behind the ear at mastoid process
• Hemotympanum
• Cerebrospinal fluid rhinorrhoea or otorrhoea
• Evidence of increasing intracranial pressure
• Decreasing level of consciousness
• Falling Glasgow coma score
• Seizure
• Cushing’s response: Bradycardia, hypertension, and diminished respiratory rate
• Dilated pupil associated with decorticates or decerebrate posture
• A dilated pupil, fall in GCS of two points or signs of cushings response indicated intracranial bleed or
swelling. These patients should be transferred only after resuscitation.
Investigation
• CBC
• Blood grouping
• Blood sugar
• CT head
• Indications for CT head
• Recent intracranial lesion seen on CT
• Persisting coma after initial resuscitation
• Confusion which persists for > 4 hours
• Progressive focal neurological signs
• Seizure without full recovery

• Depressed skull fracture

• Definite or suspected penetrating injury
• CSF leak or other sign of base of skull fracture
Management
• Cervical spine precaution
• ABC (secure airway if GCS < 8)
• Oxygen (high flow)
• IV access (avoid 5% dextrose)
• Catheterisation
• If raised ICP
o Elevate head of bed 20-30 degree
o Mannitol boluses IV
Referral Criteria
• Mass lesion associated with head trauma
• Subarachnoid hemorrhage and diffuse axonal injury
• Ongoing symptoms, disorientation
• Penetrating head injury
Discharge Criteria
• Resolved symptoms
• Negative head CT
• Minor head trauma with no loss of consciousness or amnesia and normal neurological examination

Treatment of raised ICP

1. Supportive measures
a. Keep the head in a neutral position to promote venous drainage
b. Loosen any constricting bands/collars around the neck
c. Anxiolytics and antiemetics
2. Raise head of bed to 30 degrees.
3. Mannitol
a. The initial dose of Mannitol is 0.5-1g/kg IV over 15 mins.
b. 20% Mannitol contains 20g of Mannitol per 100mL
c. For example, in a 50kg patient, 1g/kg corresponds to 50g--which equals 250mL of 20%
Mannitol
d. Onset-of-action is within minutes.
e. Peak action is 1 hour
f. Duration of action is 6-8 hours
g. Following the initial dose, a common maintenance regimen (in adults) is 100-200mL of 20%
Mannitol (ie. 20-40g) IV q6h.
h. This is titrated to an osmolality <320mosm/L
i. Mannitol decreases the ICP in several ways:
i. Osmotically draws fluid into vascular space
ii. Increases renal blood flow and urine production
iii. Reduces inflammation (ie. is a free-radical scavenger)
j. Mannitol toxicity is characterized by:
i. Serum osmolality >320mosm/L
ii. Altered mental status (eg. confusion, lethargy, stupor, coma)
iii. Hyponatremia
iv. +/- Renal failure
4. Hypertonic saline (HS)
a. Optimal dosing of HS in patients with increased ICP is controversial.
b. In patients who are coning, give 150mL of 3% NS wide open.
c. For patients with ongoing increased ICP, start an infusion of 3% HS at 30mL/hour--and then
titrate to:
i. An acceptable ICP
ii. Na <150mmol/L
5. +/- Intubate and hyperventilate
a. Titrate to a PCO2 of:
i. 20-30mmHg if actively coning
ii. 35-40mmHg if not actively coning
b. Onset-of-action of hypocarbia is 30 secs.
c. Peak action is 8mins
d. Duration of action is 20-30mins
6. +/- Dilantin 20mg/kg IV
a. Dilantin can be used to reduce the risk of seizures (which can increase ICP and cause
secondary brain injury).

b. However, the true clinical benefit of this medication in this setting is controversial.
7. Propofol +/- Pentobarbital
a. The idea is to sedate the patient in order to reduce their ICP
b. Unfortunately, sedation also typically drops the MAP--which can lower the cerebral
perfusion pressure (CPP = MAP - ICP)
8. +/- Dexamethasone
a. Dex is only effective if the increased ICP is caused by vasogenic edema (most commonly
tumor-associated).
b. Steroids do not decrease ICP (or improve outcomes) in other settings
c. A commonly-used dose is Dexamethasone 4mg IV q6h
9. +/- Cooling
a. Cooling can be considered for patients with refractory increased ICP, but there is minimal
evidence for it.
b. If cooling is used, the target temperature is 32-24C.
10. Surgical options
a. External ventricular drains
b. Burrholes and/or evacuation
c. Craniectomy

Metabolic Emergencies
Contents
Diabetic Ketoacidosis (DKA) ........................................................................................................................... 132
Common precipitants of DKA .................................................................................................................... 132
Investigations ............................................................................................................................................. 132
Management .............................................................................................................................................. 132
Hypokalaemia ................................................................................................................................................ 134
Cause .......................................................................................................................................................... 134
Management .............................................................................................................................................. 134
Hyperkalaemia ............................................................................................................................................... 135
Cause .......................................................................................................................................................... 135
Management .............................................................................................................................................. 135
Admission Criteria ...................................................................................................................................... 135
Hyponatremia ................................................................................................................................................ 136
Diagnostic Algorithm for Hyponatremia .................................................................................................... 136
Presentation of Hyponatremia .................................................................................................................. 137
Treatment of Hyponatremia ...................................................................................................................... 137
Hypernatremia ............................................................................................................................................... 140
Classification of Hypernatremia................................................................................................................. 140
Treatment of Hypernatremia..................................................................................................................... 140
SIADH ............................................................................................................................................................. 142
Diagnostic Criteria for SIADH ..................................................................................................................... 142
Precipitants of SIADH ................................................................................................................................. 142
Treatment of SIADH ................................................................................................................................... 143
Cerebral Salt-Wasting .................................................................................................................................... 144
Diagnosis of CSW ....................................................................................................................................... 144
Treatment of CSW...................................................................................................................................... 144
Prognosis of CSW ....................................................................................................................................... 144
Diabetes Insipidius ......................................................................................................................................... 145
Treatment of DI .......................................................................................................................................... 145
Hypoglycaemia ............................................................................................................................................... 147
Management .............................................................................................................................................. 147
Admission Criteria ...................................................................................................................................... 147
Diabetic Ketoacidosis (DKA)

Common precipitants of DKA
• Infections
• Non compliance with treatment
• Newly diagnosed diabetes
Clinical features
• Polyuria and polydypsia
• Weight loss, weakness
• Hyperventilation, breathlessness: acidosis causes Kassmaul’s respiration (a deep signing respiration)
• Abdominal pain
• Vomiting
• Confusion, coma
Investigations
• Blood glucose: Very high
• Electrolytes and Creatinine: Hypokalaemia
• Urine for ketones: strongly positive (+++) – Please send urine ketones only if above symptoms are
present.
• Complete blood count: WBC may be elevated, can occur in absence of infection
• Blood culture for septic screening
• Chest x ray to see infection
• ABG
Diagnosis of DKA requires positive urinary ketones and arterial pH ≤ 7.35 and or serum bicarbonate ≤
15mmol/L
Management
1. ABC
2. IV access
3. NPO for at least 6 hours (gastroparesis is common)
4. NG tube, if impaired consciousness level to prevent aspiration
5. Catheterization
6. Fluid replacement
7. Potassium replacement
8. Insulin replacement

Management
DKA
Fluid Potassium Replacement Insulin
1L NS over first 30 minutes PlasmaK+ Amount of K+ Blood glucose Insulin infusion

to add in each L (hourly) mg/dl
1L NS with potassium 2 (units/hour)
< 70 Stop insulin
hourly for 8 hours < 3.5 40
70-126 0.5-1
> 3.5 20
127-200 2
1L NS with potassium 4 > 5.5 Stop K infusion 201-360 4
hourly until rehydrated >360 7
When blood sugar is < Aim for blood glucose fall of

215mg/dl start 5% dextrose 90mg/dl/hour
infusion
Keep blood glucose at 180-240 for
first 24 hours until the Ketoacidosis
resolves, maintain with 5% dextrose
infusion
If pH < 7.1 Bicarbonate should be added to 0.45% saline infused in 3 hours. Estimation of bicarbonate
amount to be infused (mEq): (8 – HCO3 ) x kg ideal body weight x 0.5
If cerebral oedema use manitol.

Hypokalaemia
• At the level above 2.0mEq/L
Total potassium deficit is 100-200mEq/L to every 1mEq.L reduction in serum potassium
• At level below 2.0mEq/L
Deficient is much higher since a significant portion of exogenous potassium is entreated by kidneys. Total
replacement dose required may be greater than estimated
Cause
• Renal
• With hypertension: Hyperaldostronism, Cushing’s syndrome, corticosteroids
• With normal or low blood pressure: Diuretics, renal tubular acidosis
• Gastrointestinal: Diarrhea, vomiting, bowel obstruction
Management
1. Increase dietary Potassium
2. Oral Potassium
• Preferable to IV therapy whenever possible
3. IV potassium
• For serious or severe weakness
• Emergency situations rate up to 40mEq/hour (Peds 0.3mEq/kg/hr)
• Less urgent situations 10-20mEq/hour
• Use central line for concentration more than 40mEq/hour
• Frequent monitoring of potassium levels when large amounts of potassium is infused
Admission criteria
• Requiring IV potassium
• Dysrrhythmias
• Serum potassium level < 2.5mEq/L
Discharge Criteria
• Asymptomatic
• Able to replace deficiency with oral medicine

Hyperkalaemia
Cause
• Ineffective elimination
• Renal insufficiency
• Drugs: ACE inhibitors, NSAID
• Addison’s disease
• Excessive release from cell
• Burn, tissue necrosis
• Excessive intake
Management
• ABC
• IV access
• Cardiac monitor
Hyperkalemia
< 7mEq/L > 7mEq/L
Treatment
• 10ml of 10% Calcium gluconate iv
No ECG Changes ECG Changes: over 10 minutes, can be repeated
Asymptomatic Tall tented T waves every 10-20 minutes until ECG
Broad QRS normalizes
Flat P waves • Salbutamol nebulisation (5-10mg)
No Treatment • 50ml 50% of dextrose with 10U plain
Symptomatic insulin over 15-30 minutes
Dysrrhythmia • 250mg of frusemide over 1 hour (if
Generalised weakness not responding)
Admission Criteria
Potassium level rising continuously
Discharge Criteria
Potassium level < 6.0mEq

Hyponatremia
Diagnostic Algorithm for Hyponatremia
1. The following algorithm may be useful for determining the etiology of hyponatremia.
2. In hyponatremic patients, sequentially look at the following:
a. Step #1 -- Serum osmolarity
b. Step #2 -- Urinary sodium
c. Step #3 -- Total body volume
Step #1 -- Check serum osmolarity

1. Hyponatremia with decreased serum osmolarity.
a. Proceed to Step #2
2. Hyponatremia with normal or increased serum osmolarity
a. Etiologies include pseudohyponatremia due to increased:
-Lipids (eg. hypertriglyceridemia)
-Proteins (eg. multiple myeloma)
-Glucose (eg. DKA)
3. The psueudohyponatremia due to increased lipids or protein is an actual lab error which falsely
lowers the reading for serum sodium.
4. The decreased serum Na seen with hyperglycemia is often also referred to as
"pseudohyponatremia," but this is a misnomer.
a. The hyponatremia seen with hyperglycemia is real
b. It is caused by interstitial water being dragged into the vasculature by the elevated glucose
c. The term "pseudohyponatremia" refers to the fact that the sodium will return to baseline
once the hyperglycemia has resolved
Step #2 -- Check urinary sodium

In patients with hyponatremia and decreased serum osmolarity:
1. High urinary Na concentration (ie. >20-40mmol/L).
a. Proceed to Step #3
2. Low urinary Na concentration (ie. <10-20mmol/L).
a. This suggests "psychogenic polydipsia" (especially if the urine volume is large).
i. Fluid intake in these patients is commonly >1L/hr
ii. Despite the dilute urine, this overwhelms the kidney’s ability to excrete free water--
leading to hyponatremia
Step #3-- Check total body volume

In patients with hyponatremia, decreased serum osmolarity, and high urinary Na concentration:
1. Increased total body volume (ie. edema) suggests the following etiologies:
a. CHF
b. Nephrotic syndrome
c. Ascites
d. Surgical third-spacing

2. Normal total body volume suggests the following etiologies:

a. SIADH
b. Hypothyroidism
c. Hypoaldosterinism
d. Primary adrenal insufficiency
e. Medications
i. ACE-i or ARBs (decrease aldosterone)
ii. Opioids (can cause ADH release)
iii. Long-term Carbamazepine use (can cause SIADH)
3. Decreased total body volume suggests:
a. Diarrhea
b. Over-diuresis
c. Cerebral salt wasting
Presentation of Hyponatremia
1. The clinical presentation of hyponatremia depends on both the rate and magnitude of the drop.
a. In acute hyponatremia, symptoms can be seen when the Na drops to <120mmol/L
b. Patients with chronic hyponatremia can tolerate much lower levels
2. Symptoms of moderate hyponatremia can include:
a. N/V
b. Weakness
c. Cramps
d. Confusion
3. Symptoms of severe hyponatremia can include:
a. Focal neurological signs
b. Ataxia
c. Coma
d. Seizures
Treatment of Hyponatremia
1. Treatment of hyponatremia depends on the underlying etiology.
2. Different treatments are required for:
a. SIADH -- See seperate file on SIADH
b. CSW -- See seperate file on CSW
c. Hypovolemic hyponatremia
d. Hypervolemic hyponatremia
e. Severe hyponatremia
Treatment of hypovolemic hyponatremia

Common etiologies include, D/V, diuresis
1. These patients require both sodium and fluid replacement.
a. Acute hyponatremia (which developed over <24-48hrs) can be corrected rapidly.
b. Chronic hyponatremia (ongoing for >48hrs) should be corrected slowly (<0.5 mmol/L per
hour)

i. Overly rapid correction of chronic hyponatremia can cause Central Pontine

Myelinolysis.
Calculating sodium replacement in hypovolemic hyponatremia

1. The goal in these patients is to slowly increase the serum Na to an initial goal of 115-120mmol/L.
2. The classic sodium replacement calculation in hypovolemic hyponatremia is as follows:
a. Base Sodium Replacement (in mmol/L) = “Desired Na” (ie. 120mmol/L) minus “Current Na”
b. Physiological Sodium Replacement = Patient Weight (in kg) x Percent TBW x Base Sodium
Replacement (in mmol/L)
i. Kilograms and Litres cancel out--leaving the desired number of mmol of sodium
replacement
c. Knowing that 1L of NS contains 154mmol of Na, calculate the amount of NS needed.
d. Finally, calculate the appropriate rate of administration
i. Replacement should generally take place over 24-48hrs (ie. avoiding increases in Na
>0.5 mmol/hr)
3. Bear in mind that the above calculations only calculate the patient's sodium deficit.
a. The patient also needs ongoing regular maintenance fluid while the Na deficit is being
replaced
4. Ultimately, the calculations above rarely work in real life--as they do not account for changes in
urine output and composition during the replacement process.
Treatment of hypervolemic hyponatremia

Common etiologies include:
a. CHF
b. Nephrotic syndrome
c. Ascites
d. Surgical third-spacing
1. Fluid restriction is the cornerstone of therapy.

2. +/- Diuretics
a. Diuretics can be trialed in an attempt to promote free-water excretion, but they may also
promote Na excretion
b. As such, serum Na must be monitored closely
Treatment of severe symptomatic hyponatremia

1. Patients with profound hyponatremia and seizures require rapid sodium replacement--typically
with 3% hypertonic saline.
a. If 3% hypertonic saline is not available, ampules of NaHCO3 can also be used.
b. The sodium concentration of:
i. 3% hypertonic saline is 513mmol/L
ii. Ampules of NaHCO3 is 1000mmol/L (ie. 10mmol of NaHCO3 in 10mL of fluid)
2. Hypertonic saline is also "classically" recommended for profoundly hyponatremic patients who are
comatose.

a. In practice, however, the risks of aggressive sodium replacement for isolated coma (ie. no
seizures) likely outweigh the benefits
b. Gradual restoration of normal serum sodium may be more appropriate in these patients
3. There are no evidence-based guidelines for the appropriate rate of hypertonic saline administration
in a hyponatremic seizing patient.
a. One common-sense approach is to give 1mL/kg boluses of 3% hypertonic saline over 5 mins
until either:
i. The seizures resolve
ii. The serum sodium reaches 115mmol/L
b. If using NaHCO3 instead of 3% HS, give 0.5mL/kg boluses until one of these endpoints is
reached.
c. If the patient is still seizing when their serum Na reaches 115mmol/L, they likely have a
different etiology for their seizure.

Hypernatremia
Classification of Hypernatremia
The clinical symptoms of hypernatremia are similar to those of hyponatremia (see above).
Hypernatremia can be classified by:
1. Volume status
2. Mechanism
Classifying Hypernatremia By Volume Status

1. Hypovolemic hypernatremia (eg. dehydration)
2. Euvolemic hypernatremia (eg. DI)
3. Hypervolemic hypernatremia
Classifying Hypernatremia By Mechanism

1. Increased water excretion
2. Decreased water intake
3. Increased sodium intake
4. Decreased sodium excretion
a. Increased water excretion

i. Renal water loss
ii. GI water loss
iii. Dermal water loss
b. Decreased water intake
i. Disorders of thirst perception
ii. Inability to obtain water
c. Increased sodium intake
i. NaHCO3
ii. Hypertonic saline
iii. Salt tablets
iv. Sodium-rich medications (eg. penicillin)
d. Decreased sodium excretion
i. Hyperaldosterinism
Treatment of Hypernatremia
1. The treatment of hypernatremia depends on the etiology and volume status:
a. Hypovolemic hypernatremia
b. Euvolemic hypernatremia -- See seperate file on "DI"
c. Hypervolemic hypernatremia
d. Grossly-symptomatic hypernatremia
2. Similar to hyponatremia:
a. Episodes of hypernatremia developing rapidly (over <24-28hrs) can usually be corrected

rapidly.
b. Episodes of hypernatemia developing over >24-28hrs should be corrected slowly (to avoid
cerebral edema).
Hypovolemic Hypernatremia
1. These patients have lost both water and sodium--but have lost relatively more water.
a. The classic etiology is dehydration
2. If these patients are unstable, matched isotonic fluids should be administered until hemodynamic
stability is achieved.
a. Isotonic fluids can be mixed by the physician using D5W and ampules of NaHCO3
3. After hemodynamic stability is achieved, virtually any type of relatively-hypotonic fluid can be used
to correct the hypernatremia.
a. The specific type (and even rate) of fluid administration is less important than ensuring that
the serum sodium does not drop by >0.5mmol/hr
4. Calcuations are available, but they rarely work in real life.
Euvolemic Hypernatremia
-See seperate topic on "DI"
Hypervolemic Hypernatremia
1. These patients have gained both water and sodium, but have gained relatively more sodium.
2. The goal is to increase sodium diuresis while retaining free water.
3. This can usually be achieved by replacing with hypotonic fluids.
Grossly Symptomatic Hypernatremia (any etiology)

1. Patient who are seizing secondary to hypernatremia require rapid free water repletion.
2. Practically speaking, D5W should be bolused until:
a. The seizure stops
b. An initial target sodium is reached (eg. 155mmol/L)
i. If patients are still seizing when their Na drops to <155mmol/L, an alternate etiology
should be sought
3. Obviously, the risk of cerebral edema with this treatment is high.
a. Patients needs to be monitored closely for signs of increased ICP

SIADH
1. Anti-diuretic hormone (aka vasopresssin, ADH) is made in the hypothalamus and stored in the
posterior pituitary gland.
a. Its primary effect is to increase the permeability of the kidney's distal convoluted and
collecting tubules to water.
b. This increases water reabsorption in the kidney--promoting excretion of a small volume of
concentrated urine.
2. ADH secretion normally increases in response to:
a. Hypovolemia (#1)
b. Hypotension
c. Increased osmolarity
3. SIADH is a CNS disorder that causes excessive release of ADH--resulting in:
a. Retention of free water
b. Production of small amounts of concentrated urine
c. Hyponatremia and hypo-osmolarity
d. Minimal change in total body volume
Diagnostic Criteria for SIADH

1. The diagnostic criteria for SIADH are:
a. Serum Na <135 mmol/L
b. Serum osmolarity <280 mmol/L
c. Urinary Na >20-40 mmol/L
d. Urinary osmolarity >100-200mosm/L
e. Normovolemia
f. Normal cardiac, renal, adrenal, hepatic, and thyroid dysfunction
g. Absence of diuretics
2. While the volume of urine in SIADH is usually low, this is not a diagnostic criterion.
Precipitants of SIADH
1. SIADH usually has a precipitant (although it may not be readily identifiable).
2. Possible precipitants include:
a. Malignancy
b. Trauma
c. CNS pathology
d. Pulmonary pathology
e. Vomiting (ie. a powerful trigger for ADH release)
f. Pain or stress
g. Surgery
3. Potential CNS precipitants of SIADH include:
a. Stroke (ie. ischemic or hemorrhagic)
b. Mass
c. Infection

d. Inflammation
e. Demyelination
4. Potential pulmonary precipitants of SIADH include:
a. Pneumonia
b. TB
c. Lung abscess
Treatment of SIADH
1. Treat the underlying etiology.
2. Fluid restrict to 1-1.5L/day.
3. Consider Lasix.
This may promote a free-water diuresis, but close monitoring is required.
4. +/- Hypertonic saline
This is generally reserved for patients with profound hyponatremia and seizures.

Cerebral Salt-Wasting
1. CSW is a rare condition that can cause hypo-osmolar hyponatremia in the setting of CNS pathology.
a. The mechanism is poorly understood
b. Onset is usually within ten days of a neurosurgical event or procedure
2. Precipitants of CSW can include:
a. SAH (#1)
b. CNS tumors
c. CNS surgery
d. Meningitis (eg. infectious, carcinomatous, fungal)
e. Encephalitis
3. CSW is characterized by:
a. Diuresis of large amounts of highly-concentrated urine
b. Hypo-osmolar hyponatremia
c. Significant dehydration
Diagnosis of CSW
1. In patients with CNS pathology, the diagnostic criteria for CSW are:
a. Hypovolemia
b. Hyponatremia and hypo-osmolality
c. Urine [Na] >40 mmol/L
d. Urine osmolality >100 mosmol/L
e. Large urinary volume is common, but is not one of the diagnostic criteria.
2. Potential distinguishing characteristics between SIADH and CSW include the following:
a. Patients with SIADH are euvolemic and usually have a small volume of urine output
b. Patients with CSW are hypovolemic and usually have an large volume of urine output
Treatment of CSW
1. Agressive volume repletion with normal saline.
2. +/- Salt tablets
Prognosis of CSW
1. Resolution of CSW usually occurs within 3-4 weeks.
2. Long-term therapy is usually not necessary.

Diabetes Insipidius
1. DI is caused by either:
a. Lack of ADH secretion by the brain ("neurogenic DI")
b. Lack of ADH effect on the kidney ("nephrogenic DI")
2. DI is characterized clinically by:
a. Diuresis of large amounts of dilute urine
b. Resultant hypernatremia and hyper-osmolarity
3. The diagnostic criteria for DI are as follows (although this varies with different sources):
a. Serum Na >148 mmol/L
b. Serum osmolality >290 mmol/L
c. Urine output >400cc/hr x >2 hours
d. Urine osmolarity <200mosm/L
4. Central (“neurogenic”) DI is caused by lack of ADH secretion from the hypothalamus/posterior
pituitary.
a. Etiologies include:
i. Cerebral trauma, neoplasm, stroke, or hemorrhage
ii. Granulomatous disease (eg. sarcoid, TB, syphilis)
iii. Infection
iv. Hypoxia
v. Congenital/Idiopathic/Familial DI
b. Cranial trauma is responsible for 20% of cases of DI.
5. Nephrogenic DI is caused by lack of renal response to ADH.
a. It can be hereditary or acquired.
b. Acquired etiologies include:
i. Medications (eg. lithium, dilantin, aminoglycosides, amphotericin)
ii. Renal disease (eg. sarcoidosis, amyloidosis)
iii. Electrolyte abnormalitites (eg. hypercalcemia, hypokalemia)
iv. Congenital disease
Treatment of DI
1. Follow serum Na and urine output closely.
2. Resuscitate patients with fluids that are relatively-well matched to their sodium concentration, but
are mildly hyponatremic (eg. NS contains 154mmol/L of Na, RL contains 130 mmol/L of Na).
3. With the chosen fluid, replace “Urine output over 2 hours minus 5%” every 2 hours.
a. This prevents dehydration, but avoids “driving” the polyuria
4. Consider Vasopressin or DDAVP for central DI.
a. Vasopressin or DDAVP may be useful for patients with central DI who have either:
i. Very significant sodium abnormalities
ii. Very significant polyuria (ie. >6-8L in a 24-hour period)
b. These agents reduce urine output--which makes fluid replacement logistically easier.
c. Vasopressin (ie. ADH) stimuates V1 and V2 receptors.
i. V1-receptor stimulation causes vasoconstriction
ii. V2-receptor stimulation causes anti-diuresis
iii. Vasopression is administered as a continuous IV infusion of 0.01-0.03 U/min (to

desired effect)
iv. Very low doses can be effective in DI
d. Desmopressin ("DDAVP") is a synthetic ADH analogue.
i. It only stimulates the V2 receptors--causing antidiuresis without vasoconstriction
ii. Its anti-diuretic properties are up to 1,000X stronger than Vasopressin's
iii. The dose of DDAVP for DI is 2ug IV q6-12h--titrated to urine output and serum
sodium
5. Treatment for nephrogenic DI is complex, and warrants Nephrology consultation.

Hypoglycaemia
Management
• ABC
• IV access
• Send blood for investigation
• Administer dextrose
• Adult 50ml of 50% dextrose IV
• Children: 25% of dextrose 2ml/kg
• Infant: 10% dextrose 2ml/kg
• Initiate continuous IV infusion of 5-10% of glucose solution
• Monitor blood sugar 4 hourly
Admission Criteria
• Recurrent hypoglycemia
• Failure of neuroglycopenic symptoms (dizziness, confusion, seizure etc) to improve after 1 hour
Discharge Criteria
• Symptoms resolved after 24 hours and Tolerating orally

Toxicology
Contents
General Management of Poisoning ............................................................................................................... 148
Toxidromes .................................................................................................................................................... 155
Primary Management of Posoining ............................................................................................................... 156
Tricyclic Antidepressant ................................................................................................................................. 156
Serotonin syndrome ...................................................................................................................................... 156
Management .............................................................................................................................................. 156
Anti psychotics ............................................................................................................................................... 156
Extrapyramidal symptoms ......................................................................................................................... 156
Management .............................................................................................................................................. 156
Benzodiazepam .............................................................................................................................................. 157
Management .............................................................................................................................................. 157
Paracetamol ................................................................................................................................................... 158
Diagnosis .................................................................................................................................................... 158
Treatment .................................................................................................................................................. 158
Beta Blocker ................................................................................................................................................... 159
Clinical Feature........................................................................................................................................... 159
Management .............................................................................................................................................. 159
Calcium Channel Blocker ............................................................................................................................... 159
Clinical Feature........................................................................................................................................... 159
Management .............................................................................................................................................. 159
Organophosphorous Poisioning (Insectisides) .............................................................................................. 160
Management .............................................................................................................................................. 160
Zinc Phosphide (Rhodenticides)..................................................................................................................... 161
Management .............................................................................................................................................. 161
Cypermethrime (Insecticides) ........................................................................................................................ 162
Management .............................................................................................................................................. 162
Mushroom...................................................................................................................................................... 163
Clinical features:......................................................................................................................................... 163
Investigations ............................................................................................................................................. 163
Treatment .................................................................................................................................................. 163
Carbon Monoxide Toxicity ............................................................................................................................. 164
General Management of Poisoning

Overview:
One of the commonest causes of admission of young adults in the medical ward in Nepal
The annual incidence of poisoning is increasing
A great challenge to the ER attending physician esp. in our country
Presentation to hospital with poisoning is usually an acute medical exacerbation of a chronic
psychosocial disorder
Apart from infections, self-poisoning is the common easily managed fully reversible conditions
Kathmandu University Medical Journal (2006), Vol. 4, No. 1, Issue 13, 100-104
UpToDate
Importance of Risk Assessment Approach:

 Management of an individual patient requires more than just understanding of the agent ingested.
 Intoxications run a discrete, dynamic and usually predictable clinical course. May require time-critical
interventions
 Attention to the principles of critical care ensures the survival of the vast majority of patients rather
than complex maneuvers such as
• Decontamination, Enhanced elimination, Antidotes
 This approach emphasizes the fundamental importance of an early risk assessment in determining a
rational approach to subsequent management
Steps of Risk Assessment Approach:

1. Resuscitation
2. Risk assessment
3. Supportive care and monitoring
4. Investigations
5. Decontamination
6. Enhanced elimination
7. Antidotes
8. Disposition
1. Resuscitation
 Always manage from Airway Breathing Circulation
o Intubation, O2, Establish IV, Cardiac monitor
 Detect & correct
o Seizure control
 Always generalised when due to toxicologic causes
 Benodiazepines first line Rx  Barbiturates 2nd line

 Phenytoin is of no use.
o Correct hypoglycemia
 Rx if BS< 70mg/dl ; 50ml of 25% dex(5ml/kg 10% in child)
o Correct Hypo/hyperthermia
 Temp > 38.5 C prompts urgent intervention
o Consider coma cocktail
 Thiamine, 50% Dex, Naloxone
o Emergency antidotes administration
 Sometimes indicated in resuscitation phase
 eg. Atropine in OP, Naloxone in opioid, NaHCO3 in TCA
2. Risk Assessment
 Start as soon as possible, only resuscitation is a greater priority
 It is a distinct quantitative cognitive step to predict the likely clinical course & potential complication
 Helps in the subsequent management steps
o Supportive care, Screening, decontamination…
 In the majority of cases it reassures the clinician that basic supportive care will be sufficient to ensure
a good outcome
I. Agents
II. Doses
III. Time since ingestion
IV. Current clinical features and progress
V. Patient factors ( Wt. & co-morbidities)
 The agent, dose & time since ingestion should correlate with patient’s current clinical status.
If not Risk assessment needs to be reviewed
 When altered mental status prevents an accurate history
– Tablet counts
– Collateral history from family and friends
– Correlation of clinical status with toxico-epidemiologic trends
Risk Assessment Clinical Features:

 Neurological examination
 Mental Status (GCS)
 Pupil size
 Muscle tone/movements
 Reflexes/clonus
 Focal signs
 Bowel sounds

 Urinary retention
 Skin
 Pressure areas
 Colour
 Sweating
 Bullae
 Evidence of trauma
3. Supportive Care and Monitoring

Good supportive care prevents complications
• Hypoxic brain injury
• Pulmonary aspiration-atelectasis
• Pressure injuries
– compartment syndromes
– rhabdomyolysis
• Urinary retention
• Acute renal failure
• Hyperthermia
• Traumatic injuries secondary to agitated delirium
• Airway Intubation
• Breathing O2 , Ventilation
• Circulation IV fluids, Inotropes , Control hypertension
• Sedation Titrate IV benzodiazepines
• Seizure control & prophylaxis Titrate IV benzodiazepines
• Metabolic Ensure euglycaemia , Electrolytes
• Renal function Adequate hydration, Haemodialysis
• General Respiratory care, Bladder care, Pressure areas, Thrombo-embolism prophylaxis, Nutrition,
Mobilisation
Criteria for Admission in ICU include requirements for:

a) Airway control/ Ventilation
b) Prolonged or invasive hemodynamic monitoring / support
c) Haemodialysis
Criteria for admission in Emergency Observation Unit:

a. Ongoing cardiac monitoring not required
b. Adequate sedation achieved
c. Clinical deterioration not anticipated

4. Investigation:
 Either as screening test or for specific purpose
 Recommended screening test :
o ECG (readily available, non invasive)
 May identify potentially lethal cardiac conduction abnormalities eg. TCA
o Serum Paracetamol level (universal analgesic;
 send at the time of presentation ; If confirmed ingestion  after 4 hrs
o Plasma Cholinesterase level ( most common in our context)
 Not correlate well with the severity of poisoning.
 A depression of 25% or more is strong evidence of excessive organophosphate
absorption.
 Serum cholinesterase level did not correlate with the total dose of atropine
Prognostic Value of Serum Cholinesterase in Organophosphate Poisoning
Nouira S. et al, CHEST.1994;106(6):1811-1814. doi:10.1378/chest.106.6.1811
 Monitoring serial levels can be used to determine a response to therapy
 Indication for other investigation:
 Used to answer specific questions
 Drug levels may refine the risk assessment or identify specific intervention thresholds
 Paracetamol
 Digoxin
 Valproic acid
 Carbamazepine
 Iron
 Salicylate
5. Decontamination
 The objective is to decrease the absorbed dose
 Not a routine intervention
 Decisions regarding decontamination are always based on the risk assessment in that particular
individual
 Human volunteer trials and retrospective studies suggest that decontamination helps some patients
 Benefit from GI decontamination is most likely when it can be performed within one hour of poison
ingestion
 GI decontamination is most likely to benefit patients that:
 Present for care soon after ingestion
 Have ingested a poison and amount suspected to be toxic
 Are symptomatic on presentation

 Do not have clinical factors (such as CNS depression) that make decontamination dangerous
 Potential risks :
o Pulmonary aspiration ; Hypoxia ; Laryngospasm; Hypothermia
o GI complication  Bowel obstruction, perforation, MW tear
o Water intoxication esp. in children
o Distraction and diversion of staff &resources from resuscitation and supportive care priorities
 Forms of GI Decontamination
o Induced emesis
• Ipecac: No role for Ipecac in management of overdoses in the ED setting
o Gastric Lavage
• The amount of toxin removed by gastric lavage is unreliable and negligible if
performed after the first hour
• Does not confer any clinical benefit when performed routinely on unselected patients
• Despite huge spread use of multiple gastric lavages for OP pesticides poisoning across
Asia, there is currently no high quality evidence to support its clinical effectiveness .
[Systematic review of controlled clinical trails of Gastric Lavage in acute OP pesticides poisoning Li Y et at
Clin toxicology (phila) 2009 Mar:47(3):179-92 ; ED , Peking Union Medical College Hospital, Chinese
Medical Academy and Pekin Union Medical college,Beijing]
o Activated Charcoal
• Benefit must outweigh risk
• Aspiration can cause severe lung injury
• In Pediatric population in Australia, from natural poisons info data, pediatric deaths
are due to 2 reasons:
1. Opiates
2. Activated charcoal aspiration
• Oral Activated Charcoal is generally the preferred method of decontamination.
• In the intubated patient AC may be given via oro- or nasogastric tube after tube
placement is confirmed.
o Whole bowl irrigation

Potentially Useful
 Iron overdose >60mg/kg
 Slow-release KCl ingestion > 2,5 mmol/kg
 Life threatening slow-release Verapamil / Diltiazem ingestion
 Lead ingestion
 Body packers
PEGLEC
500 – 2000 ml/hr via NG (25cc/kg/hr peds)

4-6 hours duration
6. Enhanced Elimination
 The objective is to move the agent away from the target organ
o at a rate much greater than achieved by endogenous elimination
o when other therapies cannot guarantee a good outcome
 Indicated in specific poisonings
 Relies on specific pharmacokinetic properties of the agent
 Multiple dose activated charcoal for
o Carbamazepine
o Theophylline
o Phenobarbitone
o Quinine
o Dapsone poisoning
o Manipulation of urinary pH
o Salicylate
o Phenobarbitone
 Haemodialysis
o Toxic alcohols
o Salicylate
o Theophylline
o Valproic acid
o Carbamazepine
o Metformin lactic acidosis
o Potassium
o Lithium
o Amanita cyclopeptide mushroom
6. Antidotes
Drugs with specific properties used to decrease or treat the effects of poisoning
All have
i. Specific indications and contraindications
ii. Methods of administration
iii. Monitoring requirements
iv. Therapeutic endpoints
v. Adverse effect profiles
7. Disposition
• Patient must be admitted to an environment capable of providing

 Adequate level of monitoring & supportive care
• Risk assessment determines:

• Appropriate duration of observation
• Time of likely maximal clinical effects
• Duration of cardiac and respiratory monitoring
• Duration of observation for seizures and / or CNS depression
• Allows early planning for appropriate medical and psychosocial disposition.
ICU Admission
Unstable patient
Potentially lethal overdose
Cardio toxic overdose
Hospital Admission
Moderately symptomatic patient with low fatality potential
A Need of Emergency Observation Unit.

 Have been established in many ED of different countries
 Ideally located adjacent to ER
 To provide short term focused goal- oriented care.
 EOU have been remarkably successful in:
 Efficient treatment in suitable condition
 Reducing total bed days
 Increasing patient satisfaction
 Reducing inappropriate discharge and lawsuit.
Never Discharge with out Psychiatric counselling .

Toxidromes
Toxidrome Representative Most common Additional findings Intervention
Agent findings
Opoid Morphine CNS depression, Hypothermia, Ventilation or
miosis, respiratory bradycardia, death Naloxone
depression may be due to
respiratory arrest
or acute lung
injury
Sympathomimetic Cocaine Psychomorot Seizure, Cooling, sedatin –
agitation, rhabdomyolysis, benzodiazepam,
mydriasis, MI, death may be hydration
diaphoresis, due to seiqure,
tachycardia, cardiac arrest,
hyperthermia hyperthermia
Cholinergic Organophosphorous Muscarinic effects Bradycardia, Airway protection
– Salivation, miosis, seizures, and ventilation.
lacrimation, respiratory failure, Atropine,
diaphrosis, paralysis. Death parlidoxime
nausea, vomiting, may be fom
urinatin, respiratory arrest,
defecatin, bronchorrhoe or
bronchorrhea seizure
Nicotinic effect –
muscle
fasciculation,
weakness
Anticholinergic Aropine Altered mental Seizure, Physostigmine,
stats, mydriasis, dysrhythmias, sedation with
dry flushed skin, rhabdomyolysis, benzodiazepines,
urinary retention, death may be cooline,
decreaed bowel from supportive
sound, hyperthermia and management
hypethermia, dry dysrhythmias
mucous
membrane
Sedative Hyptonics Barbiturates, Depressed level of Stupor to coma, Ventilatory
Benzodiazepines consciousness, depressed support
slurred speech, rspirations, apnea,
ataxia bradycardia

Primary Management of Posoining

Tricyclic Antidepressant
Properties of TCA Effect on overdose Management
Antihistamine Sedation Symptomatic
Anticholinergic Altered mental status, dry Symptomatic
Norepihephrine post synaptic Hypotension Norepinephrine
antagonist
Serotonin Serotonin like syndrome Cyproheptadine
Na channel block Wide QRS Sodium bicarbonate 1-2 meq/kg
till pH is 5.5 to 7.55
K channel block Prolong QT Magnesium sulphate
Serotonin syndrome
Clinical feature
Altered mental status, increase muscle tone, hyperreflexia, hyperthermia, intermittend body tremor, death
may be dur to hyperthermia
Management
1. Cooling
2. Sedation with benzodiazepam
3. Cyproheptadine
a. 4-10 mg po stat
b. If responding 4 mg 6 hourly for 48 hurs
c. If not responding then repeat dose in 2 hour up to total 32 mg
Anti psychotics
Extrapyramidal symptoms
1. Early onset reversible – hours to days
a. Acute dystonia – hyperkinetic movemen disorder
b. Akathsia – subject sensation of morot restlessness
2. Delayed onset reversible – days to week
a. Parkinsonism and Neuroepileptic malignant syndrome (Tetrad: Fever, Muscle rigidity,
Autonomic dysfunction, Altered mental status)
3. Irreversible – Months to years
a. Tardive dyskinesia
Management
1. Withdrawal of drug
2. Intubation and paralysis with non depolarizing agent
3. Dantrolene 0.5-2.5mg/kg then 1mg/kg 6 hourly (should not be used with calcium)

Benzodiazepam
Onset Half life Duration of action
Short acting
Midazolam 1 minute 2 hours 3 hours
Alprazolam 1 hour 3 hours 6 hours
Intermediate acting
Lorazepam 5 minutes (IV) Less than 12 hours 12 hours
Long acting
Clonazepam 1 hour 12 hour 20-80 hour
Diazepam 1 min (IV) 12 hour 20-50 hour
Clinical feature
1. Dizziness, confusion, ataxia, incoordination, coma
2. Anterograde amnesia (Lorazepam, Midazolam)
3. Respiratory depression, Hypotension
4. Propylene glycol as diluent in parentral Diazepam and lorazepam causes severe metabolic acidosis,
nephrotoxicity, hyperosmolar satate if more than 1 mg/kg/day
Management
Flumazanil 0.2 mg iv upto 3 mg (Half life 1 hour)

Paracetamol
Stage I Stage II Stage III Stage IV
Time 24 hours Day 2-3 Day 3-4 Day 5
Clinical features Anorexia, Nausea, Improvement Anorexia, Nausea, Recovery or Death
Vomiting, malaise Vomiting,
Encephalopathy,
Anuria, Jaundice
Lab Hypokalaemia Increase AST, BP, Acidosis,
Bilirubin Coagulopathy,
Renal failure,
Pancreatitis
Diagnosis
Adult: More than 10 gm or 200mg/kg as single dose or over 24 hours
More than 6 gm or 150mg/kg over 24 hours for 2 days
Acetaminophen level should be sent at 4 hours
Four hour acetaminophen level
• 200 microgrm/ml with AST more than 1000 – Mortality 5%, Hepatotoxicity 30%
• 300 microgram/ml with AST more than 1000 – Mortality 5%, Hepatotoxicity 90%
• Less than 150 microgram/ml with AST more than 1000 – Mortality 0%, Hepatotoxicity 1%
Treatment
N- Acetylcystiene
150mg/kg in 200 ml 5% dextrose over 60 minutes then
50mg/kg in 500 ml 5% dextrose over 4 hours then
100mg/kg in 1000 ml 5% dextrose over 16 hours
Monitor for Anaphylactoid reaction

Beta Blocker
Clinical Feature
• Cardiac: Hypotension, Bradycardia, Asystole, Conduction delays, Decrease contractility
• CNS: Decrease mental status, coma, seizure
• PulmonaryL Bronchospasm
Management
• GI Decontaminaiton: Activated choarcoal or Whole bowel irrigation
• Glucagon: 0.05-0.15mg/kg bous followed by 1-10mg/hour as maintenance
• Adernergic receptor agonist: Norepinephrine, Dopamine
• Hyperinsulinemia-Euglycaemia Therapy: Insulin 1unit/kg then 0.5unit/kg/hour with 50% 50 ml
Dextrose bolus and maintenance with dextrose solution (Monitor Potassium)
• Atropine for bradycardia
• Calcium: 10% of 10ml Calcium Gluconate
• Phosphodiesterase inhibitor
• Sodium bicarconate: if wide QRS
Calcium Channel Blocker

Clinical Feature
• Hypotension, Braducardia, Shock
• Cardiogenic and non cardiogenic pulmonary oedema
• Seizure, delirium
Management
Management similar to beta blocker, lipid emulsion is also helpful

Organophosphorous Poisioning (Insectisides)

• Garlic like odour
• Nuvan (Dichlorovos): Blue liquid in small glass bottle
• Metacid (Methyl parathion): White liquid in metal container
Clinical features
• Muscarinic (DUMBELLS): Defecation, Urination, Miosis, Bradycardia, Bronchospasm, Emesis,
Lacrimation, salivation
• Nicotinic: Muscle weakness, Fasciculation, Tachcardia, Cramping of skeletal muscle, Hypertention,
Hiaphoresis, Mydriasis
• CNS: Anxiety, restlessness, lethargy, confusion, coma, seizure, respiratory & CNS depression
Management
1. ABC
2. IV access: give 1-2 liters of IV fluids depending upon the amount of fluid loss
3. Decontamination:
• Wash the skin and remove the contaminated clothes if poison is spilled in the skin or in
patients with dermal exposure
• Gastric lavage only after stabilizing (and incubating a comatose) patient who arrives within
1-2 hours of ingestion of poison.
• Give activated charcoal (1gm/kg) at the end of gastric lavage and 8 hourly for 24 hours
4. Atropinization
• Give atropine 3-5 ampoules (0.5 mg each ampoule) IV stat and every 5 minutes until the
patient is fully atropinized (heart rate > 120bpm, dilated pupils, absence of wheeze in chest,
systolic BP>90 mmHg and dry mouth and axillae). A uniform improvement in most of these
parameters is essential, not in only one or two.
• In children give atropine 0.01- 0.05mg/kg/dose as required not less than 0.1mg total dose (if
total dose <0.1, give 0.1mg)
• If patient is atropinized in first dose, stop atropine and observe
• If there is no improvement double the dose of atropine each time until there is response
• Once fully atropinized, maintain by giving 20% of the total amount every hour
• Atropine Toxicity: Extreme agitation, severe flushing, very high heart rate (>120/min).
Reduce atropine by 25% and give diazepam if severe agitation
5. Cholinesterase reactivators (Oximes): Parlidoxime 1gm 4-6 hourly (or 8mg/kg/hour). In children25-
50mg/kg over 5-10 minutes, not more than 4mg/kg/min
6. Diazepam if severe agitation or seizure

Zinc Phosphide (Rhodenticides)
Clinical features
• Nausea, vomiting (Early symptoms)
• Tightness in chest, excitement, agitation, thirst, feeling of cold
• Later may develop shock, oliguria, coma and convulsion
• May develop: Pulmonary oedema, metabolic acidosis, hypocalcaemia, liver damage, bradycardia,
ST and T wave changes and thrombocytopenia
Management
• ABC
• Oxygen
• Gastric lavage within 30 minutes post ingestion
• Administration of activated charcoal mixed with water
• Admission for 48-72 hours to observe the development of delayed onset of pulmonary oedema
• Cardiac monitoring

Cypermethrime (Insecticides)
Cypermethrin is a synthetic pyrethroid insecticide used to kill insects on cotton and lettuce, and to kill
cockroaches, fleas, and termites in houses and other buildings.
Clinical features
• Type I hypersensitivity: Anaphylaxis or irritant action to the exposed mouth, lips, eyes or skin.
• Ingested in large doses it may produce neurotoxicity like, tremor, fasciculation, convulsion, coma
and even respiratory failure
• It also causes increased salivation, upper gastrointestinal bleeding, and rarely renal failure.
Management
• ABC
• Oxygen
• Secure IV line
• NG wash
• Charcoal through NG tube
• Supportive management

Mushroom
Amanita Phalloids appropriately called “death cap” accounts for the majority of cases.
Clinical features:
• Poisoning is characterized by a latent period of 6-12 hours after ingestion (range 6-48 h), during
which the patient is asymptomatic.
• Some patients may present with GI symptoms earlier than 6 hours
• At the end of this latent period, a sudden and severe gastroenteritis like illness phase occurs
• Abdominal pain
• Vomiting,
• Profuse watery diarrhea,
• Electrolyte abnormalities
• Circulatory collapse in young and elderly persons.
• This phase, which may last as long as 2-3 days, is followed by an apparent recovery phase
• Characterized by an apparent clinical improvement
• Asymptomatic rise in hepatic enzyme levels signifies the onset of hepatic necrosis
• The third phase of
• Jaundice
• Hypoglycemia
• Coma
• Multi organ and system failure followed by death
Investigations
• CBC
• Blood sugar, electrolytes, createnine
• LFT: Liver enzymes usually raises after 36-72 hours
• PT/INR
Treatment
• ABC
• Hydration
• Gastric lavage
• Decontamination with charcoal

Carbon Monoxide Toxicity

Physiology
1. Hemoglobin
a. Each molecule of hemoglobin contains four "heme groups"--each of which holds a molecule
of iron.
b. When the iron molecule is in its reduced state (ie. Fe2+), it can bind a molecule of oxygen.
c. When the iron binds a molecule of oxygen, it is oxidized to its oxidized state (ie. Fe3+).
d. When oxygen binds to any of the four heme groups, this promotes oxygen binding at the
remaining three heme groups.
i. As such, hemoglobin is usually either fully bound to oxygen ("oxyhemoglobinemia")
or is bound to no oxygen ("deoxyhemoglobinemia")
e. After an oxygen molecule leaves a heme group, the Fe3+ is reduced back to Fe2+ by the
enzyme "NADH-MetHb reductase.”
2. Unfortunately, instead of oxygen, a heme group can also bind carbon monoxide--resulting in
carboxyhemoglobinemia (COHb).
a. When CO is bound to one of the heme groups, the other three heme groups hold onto their
oxgyen molecule more tightly (ie. the Hb-dissociation curve is shifted to the left)
3. Pulse-oximetry
a. Different molecules preferentially absorb different wavelengths of light.
i. As such, the "absorption spectra" of a substance can be used to identify it
b. The absorption spectra of oxyhemoglobin and deoxyhemoglobin are different.
i. Therefore, the relative amounts of oxyhemoglobin vs. deoxyghemoglobin in a blood
sample can be determined
c. A regular pulse-oximeter uses only two wavelengths of light.
i. It can only read Hb as either "oxygenated" or "deoxygenated"
ii. Standard pulse-oximetry cannot differentiate between oxyhemoglobin and COHb
iii. Therefore, with significant COHb, a standard pulse-oximeter typically reads 100%
saturation
4. A "co-oximeter" is similar to a pulse-oximeter, but it uses >4 wavelengths of light--which allows
distinction between:
a. Oxyhemoglobin
b. Deoxyhemoglobin
c. COHb
d. MetHb/SulfHb
Carboxyhemogloblinemia (COHb)
1. Carbon monoxide (CO) is produced from incomplete combustion of hydrocarbons (HC).
a. Complete HC combustion produces only CO2 and H20
2. CO is an odorless, colourless gas.
a. It is typically only detectable in the environment using a CO detector
3. CO toxicity should be considered in any patient presenting with new-onset neurological symptoms
(especially if other people/animals in the home/workplace are also affected).
Etiologies of COHb

i. Cigarette smoke
ii. City pollution
iii. Car exhaust
iv. Space-heaters
4. Fires
a. Several materials release both CO and cyanide when they burn.
b. Concomitant cyanide toxicity should be considered in fire victims with a lactate >10mmol/L
Pathophysiology of COHb toxicity
1. CO binds to numerous substances much more strongly than oxygen--including:

a. Hb
b. Myoglobin (ie. heart tissue)
c. Numerous tissues throughout the body
d. Cytochrome aa3 (ie. an essential molecule in the electron transport chain and aerobic
metabolism)
2. Hemoglobin's affinity for CO is 240X stronger than its affinity for oxygen.
a. As such, once bound to Hb, CO will only dissociate off in the pulmonary capillaries (because
of competitive binding by oxygen).
b. This process is relatively slow on room air, but much faster when the patient is breathing
100% oxygen (see below).
c. Fetal Hb binds CO more strongly than adult Hb.
i. As such, fetal COHb levels are typically 10-15% higher than maternal levels
3. When CO binds to cardiac myoglobin, it can result in profound myocardial dysfunction.
4. Once dissolved in the plasma, CO can diffuse into numerous peripheral tissues.
a. This is likely responsible for most clinical CO toxicity
i. Tissue CO levels correlate far better with morbidity/mortality than hemoglobin-CO
levels
b. In general, prolonged exposure to low-to-moderate dose CO is much worse for a patient
than brief exposure to high-dose CO.
Symptoms of CO Toxicity
1. Non-specific CV and CNS symptoms predominate:

a. CV (eg. angina, arrhythmias, myocardial depression)
b. CNS (eg. amnesia, difficulty concentrating, dizziness, weakness, somnolence, seizures, coma)
2. Other potential complications of CO toxicity can include:
a. Hypotension--caused by both myocardial depression and systemic vasodilation
b. Rhabdomyolysis
c. Non-cardiogenic pulmonary edema
d. DIC
e. ARF
3. The CNS sequelae of CO toxicity are not simply secondary to hypoxia.

a. CO is directly toxic to the basal ganglia and hippocampus

4. Delayed neurological sequelae (DNS) are seen in up to 40% of patients with significant CO exposure.
a. The onset of these symptoms is anywhere from 3 to 240 days after recovery (although most
occur within 20 days).
i. The precise mechanism is unknown
b. Symptoms can include:
i. Headache and fatigue
ii. Variable cognitive deficits
iii. Personality changes
iv. Movement disorders
v. Focal neurologic deficits
c. Mild DNS symptoms resolve in nearly all patients by 2 months
i. Severe DNS symptoms resolve in 75% of patients by 1 year.
d. The development of DNS correlates poorly with COHb levels.
COHb Levels
1. For the reasons discussed above, COHb levels are generally a poor marker of CO toxicity.
a. They do not correlate strongly with either morbidity nor mortality
b. Nonetheless, they remain commonly cited in the literature--and are therefore discussed
below
2. Normal COHb levels are:
a. 0-3% in rural dwellers
b. 3-5% in city dwellers
c. 5-15% in smokers
3. The following "classical" COHb symptoms are frequently cited:
a. 10-20% COHb-- Headache, malaise
b. 30% -- Impaired judgment
c. 40%-50% -- Confusion, decreased LOC, possible death
d. 60% -- Seizures, cardiovascular collapse, probable death
e. 80% -- Rapidly fatal
Testing in Suspected CO Toxicity
1. EKG
2. Co-oximetry
a. Not simple pulse-oximetry (which will read the sats as 100%)
3. Lactate
4. CK and Troponin
5. CXR
Treatment of CO Toxicity
1. 100% O2

a. All patients should be given 100% O2 by NRB or ETT.

b. The half-life of COHb is:
i. 4 hours on room air
ii. 45-90 minutes on 100% O2
iii. 23 minutes on 3atm of hyperbaric oxygen
2. +/- Hyperbaric oxygen (HBO)
a. Despite its widespread use, HBO is likely not an effective treatment for CO toxicity.
b. If effective, it is only effective at reducing delayed neurological sequelae (see above)
i. It is not a life-saving measure

Common Problems
Contents
Alcohol Intoxication ....................................................................................................................................... 168
Alcohol Withdrawal ....................................................................................................................................... 170
Diagnosis Nomenclature ............................................................................................................................ 170
Diagnosis, Initial Assessment and Investigations ...................................................................................... 170
Investigations ............................................................................................................................................. 171
Management .............................................................................................................................................. 171
Criteria for Ambulatory Detoxification ...................................................................................................... 172
Disposition ................................................................................................................................................. 172
On follow up at Alcohol clinic .................................................................................................................... 172
Motivational Interview .............................................................................................................................. 173
If not improving.......................................................................................................................................... 173
Dyslipidemia ................................................................................................................................................... 174
Diagnosis Nomenclature ............................................................................................................................ 174
Diagnosis, Initial Assessment and Investigation ........................................................................................ 174
Investigations ............................................................................................................................................. 175
Management .............................................................................................................................................. 175
Antibiotics Protocol........................................................................................................................................ 179
Undifferentiated Fever in Adult Patients................................................................................................... 179
Upper Respiratory Tract Infections............................................................................................................ 179
Urinary tract infection................................................................................................................................ 180
Alcohol Intoxication
It is important to remember that sick patients drink alcohol (to numb the pain) and people who drink
alcohol frequently become ill.
The diagnosis of alcohol intoxication is therefore a diagnosis of exclusion.
Differential diagnosis: Head injury, other toxin, hypoglycemia, drug toxicity, extreme vertigo, psychosis,
sepsis including meningitis, hepatic encephalopathy.
THINGS THAT COMMONLY KILL THESE PATIENTS
1. Airway problems (respiratory depression, aspiration)

2. Hypoglycaemia
3. Associated injury/ illness or toxin
4. Hypothermia
• Patients who have drunk alcohol are difficult to assess, often aggressive or uncooperative,
frequently unkempt or smell bad. They will test your medical skill, your compassion and your
professionalism to the limit.
• Emergency medicine involves treating substantial numbers of patitents with alcohol related illness
and injury. Most ward based jobs do not. ED staff must accept the challenge of the special role.
Effects
Alcohol produces effects to anesthetic agents.
Blood level mg%
50-100 Impaired co-ordination
100-150 Difficulty with gait/balance
150-250 Lethargy, difficulty sitting
300 Coma
400 Respiratory depression
Peak alcohol levels occur usually 30-40 minutes after ingestion
• Rapid absorption from the stomach makes washouts of little value.

• Put them on a trolley with sides, have them in the recovery position at all times. If they need the
toilet give them a bed pan or have them accompanied.
• Take a rectal temperature and commence warming measures of below 95 degrees F
• Site an IV line, push 50mls of 50% dextrose then start a dextrose drip 6 hourly
• Give 100mg of IV thiamine
• Ask for, or do yourself, hourly observations of GCS, pulse, temperature and respiratory rate.
• If the respiratory rate goes below 12 consider the intubation and ventilation may be required
• If the GCS if falling, or if the patient fails to regain consciousness after 6 hours then the diagnosis of
alcohol toxicity is probably wrong and should be reviewed.
ROAD TEST
Before discharge from ED you must be convinced that a patient who comes alone can travel home without
further injury. He/she must therefore
• Be able to walk steadily

• Be lucid
When you discharge the patient you should, if patient presented with severe intoxication
1. Assess the possibility that patient will develop delirium tremens. If this is already frank then admit
the patient. Otherwise prescribe 10-20 mg Diazepam, four times per day orally for those who
consider a
2. t risk.
3. Make a follow up arrangement in OPD for three days later where the possibility of chronic alcohol
abuse can be dealt with.
RESTRAINT
Intoxicated patient frequently cause trouble. A calm and friendly approach is least likely to end in the
patient becoming violent.
It may be necessary to tie the patient. Tie all four limbs to a trolley with the patient prone (on his/her face)
to prevent or biting. 2.5 mg haloperidol may be additionally required.

Alcohol Withdrawal
Diagnosis Nomenclature
Diagnosis CIWA Ar Other

Score Diagnosis
Alcohol Abuse/Uncomplicated Alcohol Withdrawal/ Withdrawal Seizure/Alcoholic Score HTN, DM etc

Halllucination/DT
e.g: Alcohol Withdrawal Seizure, CIWA Ar 18 with Hypertension
Diagnosis, Initial Assessment and Investigations

Alcohol abuse
Alcohol abuse is pattern of alcohol use associated with one or more of the following:
• Failure to fulfill role obligations (eg, at work, school or home)
• Recurrent substance use in physically hazardous situations
• Recurrent legal problems related to substance use
• Continued use despite alcohol-related social or interpersonal problems
Alcohol dependence
Alcohol dependence is pattern of use associated with three or more of the following:
• Tolerance
• Withdrawal
• Substance taken in larger quantity than intended
• Persistent desire to cut down or control use
• Time is spent obtaining, using, or recovering from the substance
• Social, occupational, or recreational tasks are sacrificed
• Use continues despite physical and psychological problems
Withdrawal
Uncomplicated Alcohol Withdrawal
• Insomnia
• Tremulousness
• Mild anxiety
• Gastrointestinal upset; anorexia
• Headache
• Diaphoresis
• Palpitations
Withdrawal Seizure
Withdrawal-associated seizures are generalized tonic-clonic convulsions that usually occur within 12 to 48
hours after the last drink, but may occur after only two hours of abstinence. The seizures occur
predominantly in patients with a long history of chronic alcoholism.

Alcoholic Hallucination and Delirium Tremens
Features Alcoholic Hallucination Delirium Tremens
Onset 12-24 hours 24-48 hours
Resolves 24-48 hours 7 days
Clouding of consciousness Present Absent
Hallucination Usually Visual Auditory and Tactile
Vital signs Normal Tachycardia, hypertension, fever,

agitation, and diaphoresis
Investigations
• Complete blood count, serum electrolytes, glucose, liver function and renal function tests,
urinalysis
• Premenopausal women should have an HCG test.
• An EKG is suggested for patients over 50 years, or if there is a history of cardiac problems. A chest x-
ray may be indicated for patients with chronic respiratory problems or respiratory symptoms.
Management
Minor withdrawal Diazepam 10 to 20 milligrams orally

OR Chlordiazepoxide 50 to 100 milligrams orally
OR Lorazepam 2 to 4 milligrams IV every 1 to 2 hours until CIWA-Ar scores are
<8
Withdrawal seizure Lorazepam 2 mg IV to prevent recurrence
Withdrawal Haloperidol
Hallucination
Delirium Tremens Initial Doses

• Diazepam 5 mg at 2.5 mg/min iv
• OR Lorazepam 1-4 mg every 5 to 15 min iv
Increasing Doses
• Repeat in 5-10 min then 10 mg for third and fourth dose iv
• OR Lorazepam 1-4 mg every 5 to 15 min iv
Maintenance
• 20 mg for fifth and following dose until light somnolence then 5-20 mg
per hour as needed
• OR 1–4 milligrams as needed

Adjunct
• Haloperidol 0.5-5 mg iv
Increasing dose
• Haloperidol 0.5-5 mg every 30 to 60 min
Thiamine 100 mg iv
Ambulatory Diazepam or Lorazepam on tapering dose over 7 days

Detoxification Supplementation of Thiamine
Criteria for Ambulatory Detoxification

• CIWA scores of 8 to 15 or in withdrawal stages 1 or 2, ie, without symptoms of delirium tremens
(DT): fever, disorientation, seizures, drenching sweats, or severe tachycardia or hypertension
(patients with CIWA scores >15 or DTs should be hospitalized for more aggressive treatment and
careful monitoring)
• Able to take oral medications
• Has a reliable family member or close contact who can stay with the patient throughout the
detoxification period (usually three to five days) and monitor the patient for worsening symptoms.
• Able to commit to daily medical visits
• No unstable medical condition
• Not psychotic, suicidal, or significantly cognitively impaired
• Not pregnant
• No concurrent other substance abuse that may lead to withdrawal (ie, sedative withdrawal)
• No history of DTs or alcohol withdrawal seizures
Disposition
• CIWA-Ar score <8 — Detoxification may not be needed. Follow up in alcohol clinic.
• CIWA-Ar score 8 to 15 — Patient may a good candidate for ambulatory medical detoxification, if he
or she meets specified criteria or can be admitted to GPU for observation
• CIWA-Ar score 8 to 15 - With withdrawal seizure and is stable at emergency can be admitted to
GPU for observation
• CIWA-Ar score >15 - Psychiatric referral for admission
On follow up at Alcohol clinic

Assessment of at risk drinking
• Greater than 14 drinks per week or four drinks per occasion for men
• Greater than seven drinks per week or three drinks per occasion for women
• Evaluation of stage of change (Need to document on each visit)
o Precontemplation: Not thinking of quitting
o Contemplation: Accepting need of quitting
o Preparation: Makes plan to quit
o Action: Acts on plan to quit
o Maintenance: Quits

o Relap: Starts again

Motivational Interview
Four-session, brief-contact intervention based on MI involving comprehensive assessment of drinking and
related behaviors and feedback
Four Basic Skills of Motivational Interview (OARS)
1. Open ended Question: Questions that cannot be answered with limited response like “Yes”, “No”
2. Affirmations: Acknowledging positive behaviour and strength
3. Reflective listening: Paraphrasing comments by repeating back what they have said
4. Summary statements: Putting together what they have said
Five principles of motivational interview (DEARS) - Sample questionnaire in appendix

1. Develop discrepancy: Creating the gap between where the person has been and where is he/she
now.
2. Express Empathy: Listening to get their ideas and concerns. When people feel to be understood,
they are more likely to open up to share experiences
3. Amplify Ambivalence: Ambivalence to change is normal. However it can be paralyzing and causes
some people to stuck. By verbalising and recognising ambivalence you help people to acknowledge
their ambivalence by discussing it with them and and exploring two different sides they are dealing
with, which can help them work through it.
4. Roll with resistance: Forcing, threatening and imposing will not work. Resistance is a tell tale sign
for interviewer to respond differently. Encourage people to come up with their own solution.
5. Support self efficacy: Person’s belief in understanding that change is possible is important
motivator in making change. There is no right way. Specific plan for change may not work. People
may come with different plan.
If not improving
Referral for CBT or Anti craving therapy

Dyslipidemia
Diagnosis Nomenclature
Diagnosis ASCVD Risk Statin or non statin Other Diagnosis
Score therapy
Dyslipidemia ( ASCVD Risk = Not started DM, HTN, Metabolic
LDL, HDL) 8% For primary prevention Syndrome etc
For secondary prevention
e.g. Dyslipidemia ( LDL, HDL) with ASCVD Risk Score 8% on Statin therapy for primary prevention with
Metabolic Syndrome
Diagnosis, Initial Assessment and Investigation
• Screening recommended for Age more than 20 years
• Identification of four statin benefit group
1. Individual with clinical ASCVD (Atherosclerotic cardiovascular disease)
2. Individual with primary elevations of LDL-C ≥ 190mg/L
3. Individuals 40 to 75 years of age with Diabetes with LDL-C 70-189mg/L
4. Individuals without clinical ASCVD or diabetes who are 40-75 years of age with LDL-C 70-
189mg/L and estimated 10 years ASCVD risk of 7.5% or higher
• ASCVD risk calculators are available online or application stores. Alternatively score sheet given in
appendix can be used.
• Causes of secondary dyslipidemia to be evaluated
o Diabetes
o Hypothyroidism
o Obstructive liver disease
o Chronic renal failure
o Drug that increases LDL-C, and decreases HDL-C (Progestins, anabolic steroids and
corticosteroids)
• Evaluation for Metabolic Syndrome
Risk Factor Defining Level
Abdominal Obesity
• Men • >102 cm (>40 in)
• Women • >88 cm(>35 in)
Triglycerides ≥ 150mg/dl
HDL Cholesterol
• Men • <40mg/dl
• Women • <50mg/dl
Blood Pressure ≥130/85mmHg
Fasting Glucose ≥110mg/dl
For Diagnosis – Any 3 of the above

Investigations
o Fasting Lipid profile (Non HDL C = TC – HDL C) – On each followup
o CK – Initially before starting statin and during therapy if muscle aches
o ALT – Initially before starting statin and during therapy if signs of hepatotoxicity
o HBA1C and FBS – Initially and in one to two year if stable
o TSH – Initially and as required
o Uric acid (If planning to start non statin )
o Investigate for Nephrotic Syndrome and Pancreatitis if very high TG
Management
Statin Therapy
Statin Intensity High Moderate Low
Target Daily dose lowers LDL- Daily dose lowers LDL- Daily dose lowers
C on average, by C on average by LDL-C on average by <
approximately ≥ 50% approximately 30% to 30%
< 50%
Dose Atorvastatin 40-80 mg Atrovastatin 10-20 mg Simvastatin 10 mg
Alternatively if initial value of LDL-C is not available then following target level can be used (Less evidence)
o For patients at moderate ASCVD risk
 Non-HDL-C levels of below 130 mg/dL
 LDL-C levels of below 100 mg/dL,
o For high ASCVD risk
 Non-HDL-C levels of < 100 mg/dL and
 LDL-C levels of < 70 mg/dL

Statin Therapy for ASCVD prevention

ASCVD Statin Benefit Group
In individual not receiving cholesterol lowering therapy, recalculate estimated 10 y ASCVD risk every 4-6 year in individual
aged 40-75 years without clinical ASCVD or diabetes and with LDL-C 70-189mg/dl
Age ≤ 75y
High intensity statin
(Moderate intensity statin if
Ye not candidate for high
Age > 21 years and intensity)
Clinic
candidate for Statin therapy al
Age ≥75y or if not if not
Ye candidate for high intensity
No statin
Moderate intensity statin

LDL-C ≥ (Moderate intensity statin if not
Ye
190mg/dl candidate for high intensity)
No
Ye Moderate intensity statin

DM Type 1 or
2
Age 40-75y Estimated 10 y ASCVD
Ye risk ≥ 7.5%
No
Estimate 10 y ASCVD risk
≥ 7.5% estimated 10y ASCVD Ye

Moderate to high
and age 40-75 y intensity statin
No
ASCVD prevention benefit therapy

may be less clear in this group

Management of Hypertriglyceridemia (AAFP 2007)

Borderline high TG (155-199 mg/dl)
• Work on reaching LDL-C goal
High TG (200-499 mg/dl)
• If LDL-C goal is met – Consider adding fibrate, niacin, or fish oil
• If LDL C goal is not achieved – Add increase or switch statin until LDL-C goal is achieved
Very high TG (More than 500mg/dl)

• Add fibrate or niacin
Medication Details
Drug class Agent and daily Lipid/Lipoprotein Side effects Contraindications
dose effect
HMG CoA Atorvastatin (10- LDL - 18-55% Myopathy Absolute- Acute
Reductase 80mg) HDL- 5-15% Increase liver or chronic liver
Inhibitor TG- 7-30% enzymes disease
Concomitant use
of certain drugs*
Bile salt Cholestyramine LDL - 15-30% GI distress Absolute- TG >
sequestrants (4-16 g) HDL- 3-5% Constipation 400mg/dl
TG- No change or Decrease Relative-
increase absorption of TG>200mg/dl
other drugs
Nocitinic acid Immediate LDL - 5-25% Flushing Absolute- Chronic
release – 1.5- HDL- 15-35% Hyperglycaemia liver disease,
3gm TG- 20-50% Hyperuricaemia severe gout
Extended Upper GI distress Relative –
release- 1-2gm Hepatotoxicity Diabetes,
Sustained Hyperuricaemia,
release- 1-2gm Peptic ulcer
disease
Fibric acids Gemfibrozil – LDL - 5-20% Dyspepsia Absolute- Severe
600mg BD (May increase in Gall stone renal disease,
Fenofibrate – patient with high Myopathy Severe hepatic
200mg TG) disease
HDL- 10-20%
TG- 20-50%
*Macrolid antibiotics, Anti fungal agent, Cytochrome P450 inhibitor (Niacin and Fibrates should be used
with great caution)
Dietary Advice
• Emphasize intake of vegetables, fruits, and whole grains

• Include low fat dairy products, poultry fish, legumes, non tropical vegetable oil and nuts
• Limit intake of sweet, sugar, beverages and red meat
• Reduce saturated fats and Trans fats
• Lower sodium intake, no more than 2400mg/day
Exercise
• Moderate to severe intensity aerobic exercise
• 3 to 4 session in a week
• Each session lasting 40 minutes
On follow up
Indicators of anticipated therapeutic response and adherence to selected statin intensity
• High intensity statin therapy reduces LDL-C approximately ≥ 50% from the untreated baseline
• Moderate intensity statin therapy reduces LDL-C approximately 30 to < 50% from the untreated
baseline
Access medication and lifestyle adherence – Fasting lipid panel

• If anticipated therapeutic response achieved then follow up in 3 to 12 month
• If less than anticipate response
o Access for intolerance and if present management of intolerance
o If no intolerance
• Exclude secondary cause and or
• Reinforce adherence and or
• Increase statin therapy and or
• Addition of non-statin therapy
• Follow up 4-12 week
• Decreasing statin therapy can be considered when two consecutive values of LDL-C levels are
below 40mg/dl

Antibiotics Protocol
Undifferentiated Fever in Adult Patients
Documented fever of 38° or more for 3 or more days with no clear focus of infection on preliminary
physical examination and laboratory tests. If patient is in shock or is septic, disregard this guideline.
First choice
• For non diabetics and age below 50
• Gatifloxacin 10 mg\kg\day, OD, for 7 days. Needs consultant’s co signature.
Second choice
• Azithromycin 20 mg\kg\day not exceeding 1 G OD for 7 days.
Third choice
• Ofloxacin or Levofloxacin 20 mg\kg\day for 7 days in 2 doses.
Upper Respiratory Tract Infections
1. Patients presenting with predominant nasal symptoms (nasal discharge, blockade/stuffiness, itching)
with or without cough, throat discomfort, fever and myalgia and duration less than five days: No
Antibiotics, review again in 3 days.
2. Patients presenting with predominant throat pain and fever WITHOUT nasal symptoms: Consider
antibiotics only if throat examination reveals pharyngeal or tonsillar exudates
3. Patient with progressive or persistent nasopharyngeal symptoms as in '1' above and duration more
than 5 days: consider Antibiotics (Azithromycin preferred to cover adult pertussis and atypical
organisms as well)
4. Persistent fever and dry cough with no localizing signs: treat as 'undifferentiated febrile illness' (refer
to 'fever' protocol)
Choice of Antimicrobial
1. Cap Amoxicillin 500 mg thrice daily for 10 days
2. Tab Azithromycin 500 mg daily for 5 days (if penicillin allergic)
(Applicable only in hemodynamic ally stable patients)

Urinary tract infection
Uncomplicated UTI
(Otherwise well patients without major comorbidities who are not pregnant, not recently hospitalized, not
catheterised and not thought to have any abnormal urinary tract anatomy and with normal renal function(
GFR< 60ml/min)
Acute cystitis
 Absence of fever, flank pain or any other signs and symptoms of pyelonephritis
 Able to take oral meds
Any one of the recommended antibiotics can be used:
1st choice
Nitrofurantoin monohydrate 100mg tid for 5 days
2nd choice
Trimethoprim sulfamethoxazole 160/800 mg bid for 3 days
Acute pyelonephritis
If hospitalization is required Flouroquiolones or Aminoglycosides should be used
• Ciprofloxacin 500 mg bid for 7 days
OR
• Levofloxacin 750 mg od for 5-7 days
Pregnancy
1st choice
Nitrofurantoin 100 mg tid (avoid in 3rd trimester)
2nd choice
Cephalexin 500 mg bid
 All are category B drugs

 Should be taken for 7 days
 Amoxicillin is not recommended for empirical use however can be used if culture sensitivity is
present.

Environmental Injuries
Contents
Burn ................................................................................................................................................................ 181
Electrical injuries ............................................................................................................................................ 183
Rabies ............................................................................................................................................................. 184
Burn
Introduction
Burn may be flame, liquid, chemical or electric.
Clinical features
• First degree burn:
• Involves epidermis only
• There is local Erythema and pain only
• Healing occurs in several days
• Second degree burn:
• Involves epidermis and dermis sparing portion of dermal appendages.
• Here skin is erythematous, moist, often with blister and bullae.
• Deep partial thickness burn may have blanched, white areas and thick wall blisters. Sensation is
intact
• Heals in 2-6 weeks
• Third degree burn:
• Destroys epidermis, dermis including dermal appendages
• Appears white and leathery
• Thrombosed blood vessels or skin charring may be visualized
• Wounds are insensitive
• Inhalation injury
• Facial burns
• Carbonaceous sputum
• Pharyngeal congestion
• Wheezing
• Hoarseness of voice
Investigations
• Blood glucose
Management
1. ABC: Patient with upper airway injury needs early intubation
2. IV access
3. Oxygen
4. Catheterization
5. Adequate analgesia: Morphine
6. Burn assessment

* In case of child, patient’s palm can be used to calculate % body surface area (e.g area of palm = 1%)
• Fluid Management
Parkland formula: 2-4ml of RL/NS x Body weight x % of body surface area burn. Half of the
fluid in first 8 hours and next half in 16 hours
Admission Criteria
• Partial thickness burn of non critical areas (eyes, ears, neck, hand feet or perineum) involving 10-
20% of body surface area in adult older than 10 years and younger than 50 years
• Partial thickness burn of non critical areas involving 5-10% of body surface area in children younger
than 10 years.
• Second or third degree burn involving > 10% of body surface area in patient younger than 10 years
and older than 50 years
• Second or third degree burn involving > 20% of body surface area in any patients
• Third degree burn involving > 5% of body surface area
• Significant burn of face, hands, feet, genitalia, perineum or major joints
Discharge criteria
• Patient not meeting above criteria

Electrical injuries
Introduction
Alternating current (AC):
• Found in residential power supply
• Can cause tetanic muscle contraction prolonging contact
• More likely results in ventricular fibrillation
Direct current (DC):
• Tends to throw patient from the source
• More likely to result in asystole
Clinical features
• Cardiac arrhythmias
• Respiratory arrest due to brain injury
• Altered mental status, Seizure, Coma
• Compartment syndrome
• Renal failure
• Thermal burn
• Other associated injuries due to falls
Investigations
• ECG, C spine x ray
• Urine for myoglobinuria
• Troponine I /CPK MB
• Electrolytes, Creatinine,
Management
• ABC
• Oxygen
• Spinal Immobilization
• IV fluids to maintain urine output of 1ml/kg/hour
• Catheterization
• Tetanus prophylaxis
• Local wound care
Admission criteria
• Documented loss of consciousness
• Arrhythmia, Myocardial infraction
• Suspicion of deep tissue burn
Discharge criteria
• Minor, low voltage injury (<240 v) with no associated injuries and normal ECG

Rabies
Class Definition Anti Rabies Vaccine Immunoglobin
I In contact with body fluids of Not needed Not needed
infected or suspected but does
not have breech in skin
II In contact with body fluid of Start ARV. If the animal survives Not needed
infected or suspected animal and > 10 days or laboratory
has breech in skin confirmation of no rabies, ARV
can be stopped
III Bitten by infected or suspected Start ARV. If the animal survives Recommended
animal breeching skin or infected > 10 days or laboratory
saliva gets in contact with eyes or confirmation of no rabies, ARV
mucous membrane can be stopped
Rabies vaccination not needed for bite by Mouse, Monkey, cow, goat, horse etc

Orthopedic Injuries
Contents
Principles of fracture management and dislocation ..................................................................................... 185
Spinal Injuries ................................................................................................................................................. 186
Overview of fracture management ............................................................................................................... 187
Shoulder Dislocation ...................................................................................................................................... 188
Principles of fracture management and dislocation

Introduction
Before deﬁnitive treatment of a fracture is undertaken, attention must be directed to ﬁrst aid treatment,
to the clinical assessment of the patient with special reference to the possibility of associated injuries or
complications, and to resuscitation.
Fracture type
• Closed Fracture
• Open Fracture
Dislocation type
• Complete dislocation
• Subluxation: Partial dislocation
Clinical features
• Swelling, Deformity
• Wound
• Tenderness, Abnormal bony movement
• Decreased or absent range of movement of joint
• Distal neurological and vascular status should be accessed
• Other associated injuries should also be assessed
Investigation
• X ray of the affected site (trauma series e.g. C spine lateral, pelvis anterior and chest x ray posterior
anterior view is also needed in some cases)
• Hb , Blood grouping and cross matching (as fracture femur and pelvis may cause blood loss > 2lts)
Management
• ABC
• If open fracture:
• Surgical toileting
• Inj TT
• Inj Cloxacilline 1 gm iv stat
• Immobilization: fracture site including proximal and distal joints
• If dislocated: requires urgent relocation
Admission criteria
• Open fracture
Discharge criteria
• After immobilization

Spinal Injuries
Introduction
Most spinal cord injuries are produced in association with injury to the vertebral column. These can include
any one or more of the following:
• Fracture of one or more of the bony elements
• Dislocation at one or more joints
• Tearing of ligament(s)
• Disruption and/or herniation of the intervertebral disc
Clinical features
• Pain
• Weakness
• Bowel and bladder dysfunction
• Spinal Shock:
• Immediately after a spinal cord injury, there may be a physiological loss of all spinal cord
function caudal to the level of the injury
• Flaccid paralysis, anesthesia, absent bowel and bladder control, and loss of reflex activity.
• There may also be Bradycardia and hypotension
• These last several hours to several weeks
• Absent bulbocavenous reflex and decrease anal tone
• Loss of motor and sensory function loss below the lesion
• SCIWORA — Spinal cord injury without radiographic abnormality (SCIWORA) is often defined as the
presence of neurologic deficits in the absence of evidence of bony or ligamentous injury
Investigations
• X ray spine AP and Lateral
Management
• Stabilization of C spine
• ABCDE
• Stabilization of spine in hardboard
• Per rectal examination
• Secondary survey
*Patient with spinal injury should not be discharged

Overview of fracture management

Fracture Management Technique
Phalynx Strapping With adjacent finger
Metacarpal Ball bandage Place a cotton or gauze ball in hand
and bandage it in neutral position
(slight extension of wrist and MCP
joint and flexion of IP joint)
alternatively volar slab
Scaphoid Scaphoid cast Cast in neutral position extending
from MCP joint of 2nd to 5th MCP joint
and involving IP joint of Thumb to mid
forearm
Colles Colles cast Cast from MCP joint to mid Forearm
with wrist in slight flexion and Ulnar
deviation
Both bone forearm Cast Extending from MCP joint to mid arm
with elbow flexion
Around elbow Back slab Extending from MCP joint to mid arm
with elbow flexion
Shaft of humerus Collar cuff sling Collar cuff sling with free elbow
Proximal Humerus Strapping Elbow arm strapping
Clavicle Figure of eight bandage Bandage across both shoulder in a
figure of 8
Pelvis Strapping with hard board
Femur Traction
Patella Cylindrical cast Extending from malleolus to upper
2/3rd of thigh
Around knee joint Long leg cast Extending from MCP joint to upper
2/3rd of thing
Leg Long leg cast Extending from MCP joint to upper
2/3rd of thing
Ankle Boot cast Extending from MCP joint to upper
upper third of leg
Foot Boot cast Extending from MCP joint to upper
upper third of leg
Toes Strapping Strapping with another toe

Shoulder Dislocation
Overview
1) Shoulder dislocations occur most commonly in:
a. Men aged 20-30 years
b. Women aged 60-80 years
2) The pattern of shoulder dislocations is:

a. Anterior (98%)
b. Posterior (<2%)
c. Inferior (<0.5%)
d. Superior (rare)
Anterior Shoulder Dislocations

Overview
1) Anterior shoulder dislocations account for 98% of all shoulder dislocations.
2) They are most commonly caused by:
a. Holding the arm in a "Statue of Liberty" position (during sports)
b. Fall on outstretched hand (FOOSH) in elderly patients
c. Direct posterior blow (rare)
3) On examination, the prominent acromium process gives the shoulder a "squared-off" appearance.
-Axillary nerve function (both sensory and motor) should be tested in all patients
Closed Reduction of Anterior Shoulder Dislocations
There are several different methods for reducing an anterior shoulder dislocation, including:
a. Modified Hippocratic
b. Stimson
c. Milch
d. Forward Elevation Maneuver
e. External Rotation
f. Scapular manipulation
1) Modified Hippocratic
a. This was previously a common method of shoulder reduction in the ED, but it has fallen out-of-favour
because of its forceful and potentially traumatic nature.
b. In-line traction (ie. pulling) on the affected arm is countered by a sheet wrapped around the patient's
chest and pulled in the opposite direction.
2) Stimson
a. The patient lies sedated and prone--with the affected arm hanging over the side of the table attached to
a 15lb weight.
b. Reduction is usually achieved within 30 minutes.
3) Milch

a. The patient is placed supine.

b. The affected arm is moved to the overhead position (with the elbow fully extended).
c. In-line traction is applied to the arm
4) Forward Elevation Maneuver

a. Slightly abduct the arm
b. Forward-flex the arm until it is overhead
c. Increase abduction
d. Apply in-line traction to the arm
e. External Rotation (ie. my favourite technique)
-With the patient supine or seated:
-Flex the elbow 90 degrees and fully supinate the wrist
-Slowly externally-rotate the forearm away from midline (ie. 90-150 degrees away from midline)
-If still not reduced, try moving the elbow medially (ie. towards midline)
f. Scapular manipulation
-This technique attempts to reposition the glenoid instead of the humeral head
-Place the patient in the prone position, or in a seated position (leaning forward)
-Stabilize the superior of the scapula with one hand
-Push the inferior tip of the scapula medially--which lowers the glenoid rim and helps the humeral head to
slip back in
Post-reduction (Anterior Shoulder Dislocation)
1) Shoulder reduction is usually indicated by one or more of the following:

a. A "clunking" sound
b. Decreased pain
c. Increased ROM
d. Normal shoulder appearance
2) X-rays should generally be re-performed after any manipulation.
3) Following successful reduction:
a. Consider placing the arm in a sling until pain free (ie. not more than a few days)
b. Begin shoulder range-of-motion exercises on Day 1 to reduce the risk of adhesive capsulitis (aka "frozen
shoulder")
c. Tell the patient to avoid the "Statue of Liberty" position.
Complications of Anterior Shoulder Dislocations
These include:
a. Axillary nerve injury -- 5-55% of cases
b. Associated fracture (eg. Hills-Sachs, Bankart) -- Up to 50% of cases
c. Rotator cuff tears -- 10-80% of cases
d. Vascular injuries -- Rare
e. Recurrent dislocation -- Very common

1) Axillary nerve injuries (5-55% of cases)

a. These injuries are more likely in the elderly.
-Test sensation over the deltoid
-Check muscle innervation with active abduction of the arm
b. If these injuries occur, they are usually traction neurapraxias (which have a good prognosis).
2) Associated fracture (up to 50% of cases)
a. Hill-Sachs lesion (10-50% of cases)
-This is a compression fracture of the posterolateral humeral head
-It is seen as flattening of the humeral head on X-ray
b. Bankart fracture (5% of cases)

-This is a fracture of the anterior glenoid rim
c. Humeral head fractures
3) Rotator cuff tears (10-80% of cases)

a. Rotator cuff tears are especially common following primary dislocations in patients > 40yrs old.
b. They are suggested clinically by:
-Ongoing pain for >2-4 weeks
-Inability to abduct the arm (in the absence of nerve injury)
c. Diagnosis is by MRI.
d. Patients may require operative tendon and shoulder capsule repair to restore shoulder stability.
4) Vascular injuries (rare)

-The most common vascular injury in shoulder dislocation is axillary artery injury in older patients
5) Recurrent shoulder dislocation

a. This is seen in 80-100% of patients with a primary shoulder dislocation at age <30yrs.
b. The risk of recurrence:
-Decreases with increasing age at initial dislocation
-Increases with associated Hill-Sachs or Bankart lesions
c. Physiotherapy is generally not effective at reducing recurrence.
-As such, young patients may benefit from early surgical repair of capsular lesions
Posterior Shoulder Dislocations

1) Posterior shoulder dislocations account for <2% of shoulder dislocations.
-They are less common than anterior dislocations because the glenoid fossa is angled anteriorly

2) Several mechanisms can cause posterior shoulder dislocation:

a. Seizures (possibly bilateral)
b. Electrical shock (possibly bilateral)
c. Direct blow to anterior shoulder
d. FOOSH onto an adducted hand
3) 50% of posterior dislocations are initially unrecognized--with a common misdiagnosis being "adhesive
capsulitis" (ie. "frozen shoulder)
-This misdiagnosis can result in the patient has a needlessly "locked arm" for weeks-to-months
4) As with all patients with presumed shoulder dislocation, both lateral and axillary X-rays should be
performed--in addition to the AP views.
-On isolated AP views, posterior shoulder dislocation can look deceptively normal
5) Orthopedics should be consulted in-house for all posterior shoulder dislocations.
6) Closed reduction can be attempted by:

a. Placing the patient supine with the affected arm adducted.
b. Providing in-line traction of the affected arm.
c. Having an assistant apply posterior pressure to the head of the humerus.
d. If this is successful, the arm should be immobilized in abduction and external rotation.
e. If it fails, reduction in the OR (under general anesthesia) is required
7) Chronically locked posterior dislocations (ie. dislocation missed initially, joint now frozen) should be
referred to Ortho on an expedited basis for ORIF or arthroplasty.
8) Complications of posterior shoulder dislocations include:

a. Recurrence (up to 30%)
b. Fractures (eg. glenoid rim, humeral head, greater and lesser tuberosity)
c. Subscapularis tendon avulsion
d. Neurovascular injury (very uncommon)
Inferior Shoulder Dislocations (aka "Luxatio Erecta")
1) Inferior shoulder dislocations account for 0.5% of shoulder dislocations.
2) With these injuries, the humeral head is forced below the inferior rim of the glenoid--with the humeral
shaft tilted upwards.
a. The typical mechanism is hyper-abduction.
b. The patient presents with the arm locked in 110-160 degrees of abduction--with the forearm typically
above the patient and resting on their head
3) ED management involves Ortho consultation and prompt closed reduction.

4) Closed reduction is achieved by:

a. Applying countertraction (ie. placing a towel across the affected shoulder)
b. Applying in-line traction to the affected arm--followed by abduction.
5) Rarely, button-holing of the humerus through the capsule prevents reduction.

-These require ORIF
6) Complications of luxatio erecta include:

a. Joint capsule and rotator cuff tears (100%)
b. Neurapraxias of the brachial plexus (very common)
c. Associated fractures (common)
d. Long-term adhesive capsulitis (common)
e. Thrombosis of the axillary artery (uncommon)

Obstetrics and Gynecology Emergencies
Contents
Ectopic Pregnancy .......................................................................................................................................... 193
Miscarriage..................................................................................................................................................... 194
Trauma in pregnancy ..................................................................................................................................... 195
Vaginal Bleeding............................................................................................................................................. 196
Hyperemesis Gravidarum .............................................................................................................................. 197
Ectopic Pregnancy
Introduction
Any pregnancy outside uterus is known as ectopic pregnancy. It has high risk of mortality so should be
acted upon immediately.
Risk factors for Ectopic Pregnancy

High Risk Previous ectopic pregnancy
Previous tubal surgery
Tubal ligation
Tubal pathology
Current IUCD use
Moderate Risk Infertility
Previous cervicitis (Gonorrhoea, Chlamydia)
History of PID
History of multiple sexual partners
Smoking
Low Risk Previous abdominal or pelvis surgery
Early age of intercourse (< 18 years)
Clinical features
• Classical symptoms: Abdominal pain, amenorrhoea and vaginal bleeding
• Hypotention or Orthostatic Hypotention
• Adnexal, cervical motion, and/or abdominal tenderness
• Adnexal mass, and mild uterine enlargement
• Physical examination is often unremarkable in a woman with a small, unruptured ectopic
pregnancy.
Investigations
Urine for pregnancy test
USG pelvis
Blood grouping and cross matching
Management
1. General Management
a. ABC
b. IV open with wide bore canula and start NS (may need fluid resuscitation if in shock)
c. Oxygen
d. Catheterisation
e. Ensure blood arrangement
2. Specific Management: Surgery

Miscarriage
Introduction
Pregnancy that terminates before fetus reaches viable age (< 28 weeks).
Clinical features
• Per vaginal bleeding
• Pain abdomen
• Tachycardia, Hypotension
• Shock
Investigation
• Urine for pregnancy test
• Blood grouping and cross matching (if needed)
• USG abdomen
Management
1. General management
a. ABC
b. IV open with Normal saline
c. Catheterization (if needed)
d. Oxygen (if in shock)
2. Specific management
Manual Vaccum Aspiration
Miscarriage
Hemodynamically Stable Hemodynamically unstable
IV fluid resuscitation/Blood
OS closed OS Open Urgent MVA
No Active Active No Active Active

Bleeding Bleeding Bleeding Bleeding
Explain and Admit and

Discharge observe

Trauma in pregnancy
Introduction
Fetal and maternal injury specific to pregnancy is evident after the first trimester.
Abdominal findings are less evident in the gravid patient
Minor trauma can also lead to fetal injuries
Clinical features
Fetal radiation injury is less than 1
• Abdominal pain
event/1000/rad exposure
• Uterine contraction
• Vaginal bleeding Cspine and chest s rays < 0.005rad
• Contusions Femur < 0.012 rad
Investigations AP pelvis, spine, KUB 0.14-0.5 rad

• CBC IVP 0.2-0.8 rad
• Blood grouping
CT head < 0.05 rad; thorax < 1 rad;
• Urine routine
upper abdomen <3 rad; lower
• Electrolytes and creatinine abdomen /pelvis 3-9 rad
• USG abdomen
• X ray chest with abdominal shield
Management
• ABC
• Oxygen
• Place in lateral position
• IV access with normal saline ± fluid ± blood resuscitation
• Catheteterisation if needed
• Emergency C section if needed
Admission Criteria
• Vaginal bleeding or amniotic fluid leakage
• Feto maternal hemorrhage
• Abdominal pain
• Uterine contractions
• Evidence of fetal distress
• Abruption of placenta
• Hemoperitoneum or visceral or solid organ injury
• Abdominal pain or tenderness
Discharge Criteria
• Not meeting above criteria

Vaginal Bleeding
Heavy vaginal bleeding within Yes Primary Post Partum

2 weeks of child birth Less than 24 hour Hemorrhage
Secondary Post
More than 24 hour Partum Hemorrhage
No
Yes Less then 6 Yes Severe pain in abdomen Yes Ectopic

Missed one or more periods months pregnant (± peritonism) Pregnancy
No
More than 6
month pregnant Much bleeding Yes
(± some pain) Incomplete Miscarriage
No
Threatened Miscarriage
Hard painful
No uterus and shock Yes Ante partum Hemorrhage
(no PV exam)
Resuscitate, refer, and arrange USG
No
Placental Hemorrhage
Yes
Severe lower abdominal pain Consider Ectopic
No
Genital Tract cancer,
Daily bleeding for > 2 weeks, Yes cervical erosion/polyp,
or between periods ectopic, DUB, IUCD, Depo
ABC, history,
No Exam,
Yes Investigations,
Lower abdominal mass Fibroids Diagnosis and
No treatment, refer
Yes (urgent, GRC)
Regular heavy periods and anaemia Menorrhagia
No
Yes
Post menopausal bleeding Genital Tract Cancer
No
Cause unknown

Hyperemesis Gravidarum
Nausea and vomiting are common in pregnancy, occurring in 70-85% of all gravid women. Hyperemesis
gravidarum is a severe and intractable form of nausea and vomiting in pregnancy. It is a diagnosis of exclusion
and may result in weight loss; nutritional deficiencies; and abnormalities in fluids, electrolyte levels, and
acid-base balance. The peak incidence is at 8-12 weeks of pregnancy, and symptoms usually resolve by week
20 in all but 10% of patients. Uncomplicated nausea and vomiting of pregnancy is generally associated with
a lower rate of miscarriage, but hyperemesis gravidarum may affect the health and well-being of both the
pregnant woman and the fetus.
Investigations
• Urine Ketones
• USG abdomen (after admitting to ward)
Management
• Start on 10% dextrose solution to stop fat breakdown
• Anti emetics: Metoclopramide, Ondansetron, Promethazine or Prochlorperazine
• Pyridoxine
Can be admitted to ward directly

Psychiatry Emergencies
Contents
DEALING WITH VOILENT PATIENTS................................................................................................................ 198
Predisposing factors................................................................................................................................... 198
Management .............................................................................................................................................. 198
Conversion Disorder ...................................................................................................................................... 199
Testing techniques for conversion disorder .............................................................................................. 199
Management .............................................................................................................................................. 199
DEALING WITH VOILENT PATIENTS
Predisposing factors
• Delirium
• Dementia
• Epilepsy
• Brain damage (especially temporal or frontal lobes)
• Alcohol intoxication
• Drugs (Cocaine, amphetamine, opiate or sedative withdrawal)
• Functional mental illness (acute psychosis or acute mania)
• Personality disorder
Management
Concerns for cardiac arrhythmias or QTc prolongation
Yes No
History of Yes Lorazepam 2mg IV/IM or Ketamine Droperidol 2.5 mg IM/IV or Haloperidol 5
Dementia? 4mg/kg IM or 1-2mg/kg IV mg IM/IV or Lorazepam 2mg IV/IM or
Ketamine 4mg/kg IM or 1-2mg/kg IV
No Olanzepine 10 mg IM/IV or Lorazepam Droperidol 2.5 mg IM/IV or Olanzepine
2 mg IM/IV or Ketamine 4 mg IM or 1-2 10 mg IM/IV or Lorazepam 2mg IV/IM or
mg IV or Ziprasidon 0 mg IM Ketamine 4mg/kg IM or 1-2mg/kg IV

Conversion Disorder
For diagnosis following five criteria must be met.
1. A symptom is expressed in which there is a change or loss of physical function suggesting a physical
disorder.
2. The patient has experienced a recent psychological stressor or conflict.
3. The patient unconsciously produces the symptom.
4. The symptom cannot be explained by known organic etiology or culturally sanctioned response
pattern.
5. The symptom is not limited to pain or sexual dysfunction.
Testing techniques for conversion disorder

Test Techniques
Yes no test Patient closes eyes and rsponds Yes or No to touch
stimulus. No response in numb area favour
conversion disorder
Grey test With abdominal pain due to psychological factors,
the patient will close eyes during palpation. In pain
or organis basis, tha patien is more likely to watch
the examiner hand to anticipate pain.
Drop test When a patient with paralysis of nonorganic
etiology lifts a thumb, the affected limb will drop
more slowly or fall with exaggerated speed as
compared with the unaffected limb. In addition an
extremity dropped from above the face will miss it.
Corneal reflex Will be present in pseudoseizure or coma
Bell phenomenon Eyes divert upward when lids are opened, whereas
eyes remain in neutral position in true coma
Lid closing Intrue coma, lids when opened close rapidly
initially and then more slowly as lids descend.
Awake patient wll have lids stay open, snap shut or
flutter.
Management
• Confronting the patient that nothing is real is not helpful
• Correction of precipitating factor
• Patient should be reassured that no serious medical problem has been identified
• Patient should be suggested that symptom will resolve
• Referral is mandatory
• Lorazepam may help

Police Cases
Contents
Brought by Police for alcohol examination.................................................................................................... 200
Guidelines for management of police case ................................................................................................... 201
Brought by Police for alcohol examination

1. Do the usual full examination including vitals and make sure to full undress the patient in order not to miss
anything.
2. Give any immediate care dictated by the ABC of Emergency Medicine.
3. Consider and exclude all alternative diagnosis before you make the primary diagnosis
4. Asses the degree of intoxication according to the following
Not Intoxicated Walks and Talks Slurs and Staggers Prone and Groans
No smell of alcohol Breath smells of alcohol Breath smells Breath smells
Lucid Slightly slurred speech. Speech slurred but No verbal response or
“”Happy” intelligible unintelligible speech
Normal gait Walks in straight line Ataxic but stands Can’t stand. Difficulty
without assistance sitting or coma.
Discharge Discharge to care of Admit to observation
responsible adult or ward.
police. If none, keep till IV glucose and
passes road test thiamine, restrain
hourly observation,
examine to exclude
other diagnosis.
Discharge to police only
if they sign AMA
2. Prone and Groans: These patient are severely intoxicated and at risk of death from hypoglycaemia,
hypothermia, aspiration etc. They need an aggressive approach in order to preserve their life.
Ask the patient how much they have drunk

Assess verbal response
Assess gait
Categorize as follows
1. Not intoxicated
2. Mildly intoxicated (Walks and talk)
3. Moderately intoxicated (Slurs and staggers)
4. Severely intoxicated (Prone and moan)

Guidelines for management of police case

Police case include
1. Physical assault
2. Poisoning
3. Hanging or attempted hanging
4. Drowning
5. Any kind of accident
6. Alcohol ingestion (driving and involvement in unsocial activities)
7. Sexual assault
8. Criminal abortion
Police may bring the patient to the hospital. If not they should be informed to hospital police.
Death from any of the causes given above
The body should be handed to the police not to relatives or friends.
When should a death certificate be issued?
Death certificate should be issued in all natural death
When should a death certificate be withheld?
In all police cases or suspected cases mentioned above, death certificate should be withheld and dead
body should be handed over to the police
Dead on Arrival (DOA)
History from party or relatives and clinical exam does not always give a clear diagnosis or illness or
accident. The ER doctor should examine the body to exclude accident, assult, poisioning etc mentioned
above. if suspicion arise inform the police and police will decide whether to take it as police case or not.
once the body is handed over to the police the police should sign with his or her full name in our DOA
register.
For legal standing (official purpose)
The usual procedure is the nearest relative should apply a request letter to issue death certificate to the
medical director or hospital director of the hospital and then only hospital should issue death certificate
mentioning date of admission and date and time of death with a copy of death certificate form signed by
respective consultant in charge or ER doctor attending the patient. one copy of this should be kept in the
hospital file or record
Police case register
ER doctor on duty must enter the following details in the patient book kept in emergency room
1. Date and time of attendance at ER
2. Full name ,age, sex and address of the patient
3. Name and signature of the person bringing the patient. If brought by police the details of
police should be written

4. Permanent NO. of hospital
5. History exam
6. Type of injury bruise, contusion, abrasion, laceration, incised wound, puncture wound,
fracture ,dislocation, internal injuries, sign of ligature etc
7. Site of injury on the body
8. Measurement of each injury
9. In sexual assault-vaginal and genital swab to be taken for examination for spermatozoa and
sent to laboratory at once and in all case of sexual assault gynecologists or surgeon should
be called to give opinion as to whether sexually assaulted or not
Discharge
When police cases are discharged the discharge office should inform the police.

Procedures
Contents
Non invasive ventilation ................................................................................................................................ 203
Maintenance of NIV ................................................................................................................................... 204
Rapid Sequence Intubation ............................................................................................................................ 206
Preparation ................................................................................................................................................ 206
Preoxygenation .......................................................................................................................................... 206
Pretreatment ............................................................................................................................................. 207
Paralysis and induction .............................................................................................................................. 207
Positioning and protection ........................................................................................................................ 207
Placement with proof ................................................................................................................................ 207
Post intubation procedure ......................................................................................................................... 207
Emergency Cricothyroidotomy ...................................................................................................................... 208
Using ventilator in ED..................................................................................................................................... 210
Capnography .................................................................................................................................................. 211
Normal Waveform CO2 .............................................................................................................................. 211
Endotracheal tube in oesophagus ............................................................................................................. 211
Endotracheal tube leak .............................................................................................................................. 212
Decerased muscle relaxan effect of breathing against ventilator............................................................. 212
Central Venous Line ....................................................................................................................................... 214
Percutaneous Cardiac Pacing ......................................................................................................................... 215
FAST................................................................................................................................................................ 216
FOCUS (Focal cardiac ultrasound).................................................................................................................. 217
Chest tube insertion....................................................................................................................................... 218
Sengstaken Blackmore tube .......................................................................................................................... 218
Procedural Sedation....................................................................................................................................... 219
Interscaleni Block ........................................................................................................................................... 220
Drug Preparation............................................................................................................................................ 221
Dopamine ................................................................................................................................................... 221
Noradrenaline ............................................................................................................................................ 221
Non invasive ventilation

Definitions
1. Respiratory Distress – Combination of signs and symptoms that include dyspnea, obtundation,
tachypnea, cyanosis and accessory respiratory muscle use, along with an inadequate exchange of O2
or CO2.
2. Impending Respiratory Failure – Clinical signs and symptoms of respiratory distress which, if left
uncorrected may lead to respiratory failure.
3. Dyspnea – Subjective symptom of breathing discomfort.
4. Respiratory Accessory Muscle Use – The use of respiratory muscles for respiration, which are
normally only used on exertion.
5. Paradoxical Breathing – Breathing movements in which the chest wall moves in on inspiration and
out on expiration, in reverse of the normal movements.
Assessment of condition/disorder diagnosis

A patient assessment will be performed by the MO. NIV is a recommended therapy for treatment of COPD,
Cardiogenic Pulmonary Edema and for therapy post extubation at high risk of recurrent respiratory failure.
NIV is indicated for a patient who is spontaneously breathing and who demonstrates clinical evidence of
respiratory distress and meets the following gas exchange/physiological criteria:
pH < 7.35
SpO2 < 90%
PaCO2 > 45 mmHg or
PaO2/FIO2 < 200
RR > 35 BPM
Contraindication
NIV is NOT recommended in the following clinical situations. If any of the following are met, intubation should
be considered:
• Altered level of consciousness
o GCS <8
o Unresponsive, unable to cooperate, or apply / remove the mask
• Impending respiratory failure
o RR<8breaths/min
o pH < 7.20
• Hemodynamic Instability
o SBP<90mmHg
• Uncontrolled arrhythmias
• Airway Obstruction
• Inability to clear secretions
• Pneumothorax, blebs and bullae
• Inadequate respiratory drive
• Unstable spine injury

Intervention
Initiationof NIV
The health care provider will explain the procedure to the patient before starting any therapy. Choose the
appropriate interface for the patient.
NIV is not a life support ventilator and is intended only to augment spontaneous breathing.
NIV is not be used invasively on tracheostomy patients.
Turn on the CPAP delivery device, perform exhalation test and attach it to the patient.
Set the initial settings at:

• IPAP = 12cmH2O
• EPAP = 8cmH2O
Titrate to ventilation needs (Clinically)
Titrate to oxygen needs (SpO2 > 90% or as ordered):

• Titrate the FiO2
Set the alarms to the appropriate levels based on set parameters.

Monitor the patient’s comfort/tolerance and make appropriate adjustments.
Maintenance of NIV
The MO will assess the ventilation and patient status at least Q3H while the patient is on CPAP. The following
parameters will be included in the assessment:
• Mode
• CPAP level
• No audible leak
• Spontaneous Rate
• FiO2
• SpO2
• HR
• BP
Within 30 minutes of initiation of CPAP an ABG is recommended. Assess for an improvement in the ABG’s
and the respiratory symptoms. If:
• No improvement – Optimize the CPAP and/or reassess the exclusion criteria, notify physician,
consider intubation. The MO may adjust NIV between 5—18 cm H2O to achieve targets.
• Improvement – Assess the patient for weaning readiness.
Patients must not be physically restrained when on NIV.

The MO will be advised of any pre-planned removal of the NIV mask for procedures. Where the removal of
the mask may compromise the patient’s ventilatory status, the MO must be present and shall provide

saturation monitoring and oxygen to maintain SpO2 > 88%.
A nasal gastric tube should be in place prior to applying face mask ventilation if any of the following occur:
• NIV exceeds 20 cm H2O
• Patient is unable to remove FM
• The patient has vomited, is predisposed to vomiting, or has GI reflux.
• If patient is unable to remove mask, the patient will remain under continuous observation.
Humidity has been proven to improve patient compliance by decreasing the drying effects of the high flow
of gas. Heat and Moisture Exchangers (HMEs) will not be used in the CPAP circuit.
Heated humidity may be added to the CPAP circuit at the MO's discretion. Humidity should be considered
when:
• Patient is expected to be maintained on CPAP for > 12hours
• Primary diagnosis is consolidation/pneumonia or COPD
• Patient is complaining of dryness/ discomfort or is experiencing nosebleeds or other symptoms of
upper airway drying.
For medication delivery, the following options are preferable:

• MDI with spacer (with or without face mask).
If the patient cannot tolerate being removed from CPAP, small volume nebulizer tee’d into the CPAP circuit
should be considered, with the consideration that this may result in a vastly reduced deposition of the drug.
Weaning of NIV
The Patient should meet the following weaning criteria before weaning NIV:
• Clinically stable
• RR < 25 BPM
• HR < 110 BPM
• pH >7.35
• SpO2 > 92% on < 50%
If the patient meets the above weaning criteria, a trial off NIV therapy on comparable FiO2 may be
considered. Post NIV removal, assess and monitor the patient’s respiratory parameters. MO may consider
ABG post discontinuation of CPAP to assess respiratory status. If the patient demonstrates clinical evidence
of respiratory distress reinstitute NIV at previous settings and optimize NIV.
Documentation
Chart all procedures done, complications, changes and respiratory assessments on the xPAP flowsheet.
Ventilation and patient status will be monitored at least Q3H while patient on NIV therapy. All measurable
and set parameters will be recorded in the xPAP flowsheet with justification for parameter changes.

Rapid Sequence Intubation

Preparation
Preparation includes assessing the patient's airway, developing an airway management plan, and
assembling necessary equipment and medications.
Airway assessment (LEMON)
Look externally: Facial deformities
Evaluate (3-3-2 rule):
• 3: This assessment indicates the ease of access to the airway. A normal patient can open his mouth
sufficiently to permit three of his own fingers to be placed between the incisors. Adequate mouth
opening facilitates both insertion of the laryngoscope and obtaining a direct view of the glottis.
• 3: This assessment provides an estimate of the volume of the submandibular space. A normal
patient is able to place three of his fingers along the floor of the mandible between the mentum
and the neck/mandible junction (near the hyoid bone).
• 2: This assessment identifies the location of the larynx relative to the base of the tongue. A normal
patient is able to place two fingers in the superior laryngeal notch (ie, the space between the
superior notch of the thyroid cartilage and the neck/mandible junction, near the hyoid bone). If the
larynx is too high in the neck, direct laryngoscopy is difficult or impossible because of the angles
that have to be negotiated to permit visualization.
Mallampati score: Class I and II are easy, III and IV are difficult
Obstruction/Obesity: Airway obstruction with supraglottic mass
Neck mobility
Difficult bag and mask ventilation
• M: mask seal – , absence of facial hair, lack of interfering substances, such as excessive vomitus or
bleeding, and the ability to apply pressure to the face with the mask.
• O: Obstruction/Obesity – Placing the bed at an angle with the head higher than the feet (ie, reverse
Trendelenburg) may reduce impedance to airflow from abdominal weight.
• A: Age – In one study, age >55 years was a marker of difficult
• N: No teeth – Edentulousness creates difficulty with BMV. Teeth provide a framework against
which the mask sits and support the cheeks, enhancing mask seal.
• S: Stiffness – “Stiffness” is used to connote resistance to ventilation that occurs in conditions that
increase the required inspiratory pressure to ventilate the lungs and include asthma, chronic
obstructive pulmonary disease (COPD), pulmonary edema, widespread infiltrates, and any other
condition that decreases pulmonary compliance.
Preoxygenation
Any patient who may require urgent tracheal intubation should immediately be given high flow oxygen at
the highest possible concentration. Alternatively, 8 vital capacity breaths may be used in cooperative
patients and will provide equivalent pre-oxygenation in less than one minute.
Apneic oxygenation is continuing oxygen in high flow through nasal prong during intubtion.

Pretreatment
Pretreatment with Lidocain can blunt reflex and prevents elevation of ICP during intubation. If patient is
very dyspneic and using bicarbonate as pretreatment might be helpful.
Paralysis and induction

Inj Ketamine 1-2 mg/kg iv (In an average 100 mg)
Inj Suxamethonium 2 mg/kg iv (In an average 100 mg)
Positioning and protection

Sniffing positon and BURP (Behind Upward Right Posterior ) pressure to thyroid cartilage
Placement with proof

Direct visualization
ETCO2
Ultrasound confirmation
Double track sign in trachea
Post intubation procedure

Positioning, taping etc.

Emergency Cricothyroidotomy
1) The cricopharyngeal membrane is only 1cm tall vertically.
2) As such, the largest ETT that should be placed through it is a Size 6.
-Remember that ETTs are sized according to their inner diameter (in mm)
Predictors of a Difficult Cricothyroidotomy -- "FOR ITCH"

a. Flexed neck
b. Obese
c. Radiation therapy
d. Infection
e. Tumor
f. Coagulopathy
g. Hematoma
Procedure
Equipment
1) Scalpel
2) Skins hooks x 3
3) Snaps x 2
4) Scissors
5) Tracheal (“Trousseau”) dilator or a Kelly
6) Size 6 cuffed ETT tube
7) Sutures or trach ties
Technique (for right-handed physicans)

1) If there is time, prep the neck with Betadine.
2) Give sedation +/- paralysis if the patient is awake and/or moving.
3) If the patient is not in C-spine precautions, hyperextend the neck.
4) Stabilize the larynx with the left hand.
5) Make a 4cm vertical midline incision in the skin over the cricothyroid membrane--thereby exposing the
membrane.
6) Place a skin hook on either side of the skin incision and have an assistant hold the field open.
7) Make a 1cm horizontal stabbing incision through the inferior cricothyroid membrane (to avoid the
cricothyroid arteries).
a. Only allow the tip of the scapel to enter the trachea
b. Avoid perforating the posterior tracheal wall
8) Before removing the scalpel, insert a Kelly into the hole.
9) After the Kelly is in place, remove the scalpel and extend the horizontal cricothyroid membrane incision
with scissors.
10) Place a tracheal hook on the superior side of the horizontal cricothyroid membrane incision and get an
assistant to hold it upwards.
11) Leaving the Kelly in place, gently insert the Trousseau dilator into the hole.
a. The Kelly will need to be gradually removed as the Trousseau dilator is inserted

b. If a Trousseau dilator is not available, use the Kelly to dilate the hole directly
12) Insert a Size 6 cuffed ETT tube into the hole.
a. The Trousseau dilator (or Kelly) will need to gradually be removed as the ETT is inserted.
b. Do not insert the ETT tube too deeply down the trachea (to avoid a right-mainstem intubation).
13) If possible (and oxygenation permits), confirm placement with a video device (eg. bronchoscopy)
before bagging the patient.
14) Inflate the ETT cuff and confirm CO2 return.
15) If not already done, confirm placement with a video device.
16) Secure the tube with sutures or a trach tie.
Complications of Cricothyroidotomy
1) The most common complications are:
a. Bleeding
b. Failed procedure
c. Incorrect site of tube placement
d. Prolonged procedure time
2) Long-term complications of cricothyroidotomy are rare.
-The most common long-term complication is dysphonia or voice change

Using ventilator in ED
Starting
• Patient’s attendant need to know that we might not have control on all parameters with this
ventilator for long period, so needs to be shifted as soon as possible.
Ventilator preparation - Cross vent 3 (biomed)

1. Check the power cable, vent circuit, exhale volume sensor, oxygen tube connection.
2. Power on with switch button
3. You can setup with setup key at monitor (Usually this step is not needed as ventilator is already in
functional mode).
4. Three knob at the bottom of ventilator: 1st PIP – set to 15 to 25 (usually 20). 2nd Knob (PEEP) – set to
5. 3rd knob (flow rate) - keep it to 60 L/min.
5. Touch Main then touch A/C mode
6. Touch Rate then change with up/down key to 14 to 16.
7. Touch TV and change with up/down key to 8-10ml/kg (450-550ml).
8. Attach the circuit of the ventilator to the ET tube.
9. If you want to change to SIMV/CPAP mode, touch SIMV/CPAP and repeat the same.
10. Make sure to sedate patient if you are using A/C mode.
Medications for Rapid Sequence Intubation

• Sedation and analgesia: Ketamine 1-2 mg/kg
• Paralysis: Succniyl choline 2 mg/kg
• Example: For 50 kg- 100 mg of Ketamine (2ml) and 100 mg of Sux (2ml)
Connect to ventilator
• Settings may change when connected to patient, so please see monitoring panel
• For monitoring panel touch Alarm 1 and Alarm 2 in monitor
• Fill up sick patient monitoring chart
Muscle Relaxation: use Vecuronium as below

• Loading: 0.05mg/kg i.v following 5 minutes of Succinylcholine administration
(e.g: for 50kg 0.05 x 50=2.5mg)
• Maintenance: 0.01-0.015 mg/kg i.v 20-45min post initial dose.
(e.g: for 50kg 0.01 x 50 =0.5 mg)
Sedation
• Midazolam 1 mg per hour and additional 1 mg as per needed in between.
• Caution: Hypotension
Analgesia
• Morphine 1 mg per hour
• Caution: Hypotension, Respiratory depression
Alternatively for sedation and analgesia

• Ketamine 0.1-0.5 mg/min iv

Capnography
Normal Waveform CO2
A-B: Zero baseline – beginning of exhalation

B-C: Rapid sharp rise – anatomical dead space gas replaced by more distal airway gass that contain more CO2
C-D: Alveolar plateau – containes mixed alveolar gases
D: End Tidal CO2 – highest concentration of exhaled CO2
D-E: Rapid sharp downstorke – inhalation phase, frsh gas rapidly replaces CO2
Endotracheal tube in oesophagus
No CO2 measured. Only small short lived capnogram displayed.

Endotracheal tube leak
If air leak around endotracheal tube cuff, alveolar (end tidal) CO2 gas is diluted. The alveolar plateau is
blunted and it bends with the downstroke of the capnogram. Look for
• A deflated or leaky endotracheal or tracheal tube cuff
• An artificial airway that is too small for patient.
Decerased muscle relaxan effect of breathing against ventilator
The cleft in the far right portionof the alveolar plateau indicates that the diaphragm is moving and is causing
entrainment of fresh air. A cleft can occur in any part of the alveolar plateau when the patient attempts to
breath against ventilator.
Cleft in capnogram (may not be on every waveform)
Humped waveform (indicating attempts at spontaneous breathing)

Endotracheal tube kinked or airway obstructed
If exhaled CO2 gas is completely or partially obstructed, the slope of the ascending limb of the capnogram
has litter or no alveolar plateau. Look for
Partially kinked or occluded artifically airway
Herniated endotracheal or tracheal tube cuff
Bronchospasm, COPD
Foreign body in upper airway
Rebreathing CO2
If the patient is rebreathing previously exhaled CO2. ETCO2 values increase and the baseline elevated. The
waveform does not return to zero at the end of inspiration. Look for
Inadequate expiratory time
Malfnctioning inspiratory valve
Malfunction of circuit
Insufficient inspiratory flow rate.

Central Venous Line

Place the patient in tendlenburg position.
Proceed in 45 degree to skin surface.
Internal jugular vein in 2-3 cm below skin, if vein not hit change direction or angle of needle.
Success rate increases and complication decreases with use of USG.

Percutaneous Cardiac Pacing

Pad placement
Pacing
• Connect cable to electrode
• Turn the output courrent dial as low as possible
• Set the pacing rate between 80 and 90 beats per minute
• Select pacer function
• Turn it on
• Gradually increase the current output to 5 to 10 mA at a time until capture is achieved.
Assessment of successful pacing

• Successful capture is usually characterized by a wde QRS complex and broad T wave.
• Electrical capture is best judged by the presence of consistent ST segment and T wave after each
generated facer spike.

FAST
Consists of 4 views
– Subxiphoid
– Right Upper Quadrant
– Left Upper Quadrant
– Pouch of Douglas
Right upper quadrant
Left upper quadrant
Pelvis

FOCUS (Focal cardiac ultrasound)

Figure 1
Figure 1
Subxiphoid view
Place the probe at subxiphoid area
pointing towards left shoulder.
Figure 2
Parasternal short axis
Place the probe at 3rd or 4th
intercoastal space with marker pointed
towards left shoulder
Figure 2
Figure 3
Parasternal long axis
Place the probe at 3rd or 4th
intercoastal space with marker pointed
towerds right shoulder
Figure 4
Four chamber view
Place the probe at apex with marker
pointed towards left shoulder
Figure 3 Figure 4

Chest tube insertion

Review
Sengstaken Blackmore tube

• Insert the lubricated SB tube until the 50 cm mark is located just outside the nares or teeth.
• Confirm its position in stomach by flushing and aspirating the port with air while auscultating over
the epigastrium
• Inflate the gastric bulb with 200 to 250 ml of air then pull back until resistance
• Apply traction and fix the tube
• Inflate oesophageal balloon to ta pressure of 25mmHg
• If bleeding continues increase the oesophageal balloon pressure in 5 mmHg increment until 45
mmHg
• If bleeding is controlled reduce oesophageal balloon pressure every 3 hourly until 25 mmHg
• Deflate oesophageal balloon for 5 minutes every 6 hourly to avoid oesophageal pressure necrosis

Procedural Sedation
Level of sedation analgesia
Minimal sedation Moderate sedation Deep sedateion General
(Anxiolysis) (Conscious sedation) Anaesthesia
Responsiveness Normal response Purposeful response Purposeful response Unarousable even
to verbal to verbal or tactile after repeated or with painful
stimulation stimulation painful stimulation stimulation
Airway Unaffected No intervention Intervention may be Intervention often
required required required
Spontaneous Unaffected Adequate May be inadequate Frequently
ventilation inadequate
Cardiovascular Unaffected Usually maintained Usually maintained May be impaired
function
Principle of procedural sedation and analgesia

• Determine appropriate level of sedation desired
• Have appropriate monitoring and rescue equipment
• Administer analgesic before sedative
• Titrate agents to desired level of sedation
• Observe and monitor until recovery to baseline mental status
Recommendation regarding fasting state in low risk patient

Fasting state Urgency Risk of aspiration Suggested sedation level
No oral intake < 3 h Any Low No limitation
Any clear liquid < 3 h Urgent Higher No limitation
Any clear liquid < 3 h Non urgent Higher Limit to moderate sedation
Light snack < 3 h Urgent Higher Limit to brief deep sedation
Light snack < 3 h Non urgent Higher Limit to moderate sedation
Meal < 3h Urgent Highest Limit to moderate sedation
Meal < 3 h Non urgent Highest Limit to minimal sedation
Sedation agent for adult procedural sedation and analgesia

Medication Dose Route Onset Duration Use
Midazolam 0.05-1mg/kg IV 1-3min 1h Minimal or moderate
May repeat 0.05mg/kg every 2 sedation
min until necessary sedation
Ketamine 1-2mg/kg IV 1-3min 10-20 min Dissociative sedation
Propofol 1mg/kg followed by 0.5mg/kg IV 1-2min 5-10min Moderate/ deep
every 3 min if needed sedation

Ketofol 10mg/ml of both medication IV 1-2 min 10-20 min Moderate and deep
(Ketamin+ mixed in1:1 sedation
Propofol) Given 1-3 ml every 2-3 min
until desired sedation is
achieved
Interscaleni Block
Review

Drug Preparation
Formula
Drug in ml/hour =(Drug dose required (mcg) x weight (kg) x 0.06)/(Drug in bag (mg)/Fluid in bag (ml)
Calculaiton of drops
Pediatric set: ml/hr = drops/min
Adult set: (ml/hr)/3
Dopamine
Dose: 5-20mcg/kg/min
Each 5 ml contains 200 mg of Dopamine
Add 5 ml Dopamine in 100 ml of NS
Dose 35 kg 40 kg 45 kg 50 kg 55 kg 60 kg 65 kg 70 kg
5mcg/kg/min 5ml/hr 6 7 8 8 9 9 10
10 mcg 10ml/hr 12 13 15 16 18 19 21
/kg/min
15 mcg 15ml/hr 18 20 22 24 27 29 31
/kg/min
20 mcg 20ml/hr 24 27 30 33 36 39 42
/kg/min
Noradrenaline
Dose: 0.01-3mcg/kg/min
Add 4ml = 4mg in 100 ml of NS
Add 4ml /100 ml of NS
Dose 50 kg-60 kg 70-80 kg
0.03mcg/kg/min 3ml/hr 4ml/hr
1mcg /kg/min 75ml/hr 120ml/hr
2 mcg /kg/min 150ml/hr 240ml/hr
3mcg /kg/min 300ml/hr 500ml/hr

Protocol for Management of Common Paediatric Problems
Department of Pediatrics
Patan Hospital
3rd edition; 2070 (2013)
222
CONTENTS
1. WHEEZING ........................................................................................................................ 225
2. STRIDOR ............................................................................................................................ 227
3. BRONCHIAL ASTHMA .................................................................................................... 229
4. TRAUMA ............................................................................................................................ 230
5. STATUS EPILEPTICUS ..................................................................................................... 232
6. COMA.................................................................................................................................. 234
7. NEUROCYSTICERCOSIS ................................................................................................. 237
8. DRUG/ FLUID DELIVERY IN A SICK CHILD ............................................................... 239
9. INITIAL ASSESSMENT OF A SICK CHILD ................................................................... 241
10. BASIC LIFE SUPPORT (AHA guideline, 2013).............................................................. 242
11. BURNS .............................................................................................................................. 243
12. CHOKING .........................................................................................................................246
13. NUTRITION REQUIREMENTS FOR CHILDREN ........................................................ 247
14. IV FLUID RESCUSITATION IN DEHYDRATION ................................................. 249
15. URINARY TRACT INFECTION ..................................................................................... 252
16. NEPHROTIC SYNDROME.............................................................................................. 255
17. MANAGEMENT OF DIABETIC KETOACIDOSIS IN CHILDREN ............................ 258
18. SEPTIC SHOCK................................................................................................................ 261
19. RECOGNITION OF MENINGOCOCCAL DISEASE..................................................... 264
20. ORGANOPHOSPHATE (OP) POISONING .................................................................... 265
21. EYE INFECTIONS ........................................................................................................... 269
22. OTHERS ............................................................................................................................ 270
I. RULES OF THUMB FOR EXPECTED INCREASE IN WEIGHT.................................................................. 270
223
II. RULES OF THUMB FOR EXPECTED INCREASE IN HEIGHT ................................................................. 270
III. RULES OF THUMB FOR EXPECTED INCREASE IN HEAD CIRCUMFERENCE ................................. 271
IV. PAEDIATRIC NORMAL VALUES FOR VITAL SIGHS ............................................................................ 271
V. NORMAL HEMOGLOBIN LEVELS.............................................................................................................. 271
VI. NORMAL BLOOD PRESSURE IN CHILDREN .......................................................................................... 272
VII. NORMAL HEART RATE IN CHILDREN .................................................................................................. 272
VIII. NORMAL RESPIRATORY RATE IN CHILDREN ................................................................................... 272
IX. APPROXIMATE AVERAGE HEIGHT AND WEIGHT FOR NORMAL CHILDREN ............................... 272
X. INTRAVENOUS FLUID REQUIREMENTS.................................................................................................. 273
XI. DAILY ELECTROLYTE REQUIREMENTS ................................................................................................ 273
XII. PLEURAL EFFUSIONS ............................................................................................................................... 273
XIII. ASCITIC FLUID .......................................................................................................................................... 273
XIV. PERICARDIAL EFFUSIONS...................................................................................................................... 274
XV. BLOOD CULTURE COLLECTION ............................................................................................................ 275
XVI. ASSESSMENT OF DEVELOPMENTAL MILESTONES ......................................................................... 276
XVII. GUIDELINES FOR PHOTOTHERAPY IN NEONATAL JAUNDICE .................................................... 280
XVIII. GUIDELINES FOR EXCHANGE4 TRANSFUSION IN NEONATAL JAUNDICE .............................. 281
XIX. NORMAL VALUES FOR THYROID FUCTION TESTS IN CHILDREN ............................................... 282
XX. INDICATIONS FOR PICU ADMISSSION .................................................................................................. 282
224
1. WHEEZING
First wheezing & severe respiratory distress
• Start oxygen
• Give salbutamol nebulization (< 2years: 0.2 -0.6 mg/kg/day divided q4-6 hourly, > 2years:
0.6-2.5 mg 4-8 hourly)
• A trial of epinephrine nebulization can be given if bronchiolitis is suspected
• No CXR or blood tests in ER
• Pediatric resident will likely admit and decide if CXR and blood tests are needed
• Avoid IV lines in children <5 years if possible (it may cause un-necessary agitation); at least wait
until trial of bronchodilator
Recurrent wheezing and severe respiratory distress

• Immediate oxygen
• Immediate continuous salbutamol nebulization for 1 hour
• Ipratropium nebulization)
• Steroids: hydrocortisone 10 mg/kg IV (max 200 mg) or oral prednisone 2 mg/kg (max 60 mg).
o Children who do not require intravenous access for other reasons should receive systemic
glucocorticoids orally. Oral administration is preferred because it is less invasive and the
effects are equivalent.
o Intramuscular administration of glucocorticoids may be warranted in patients who vomit orally
administered glucocorticoids, yet do not require an intravenous line for other purposes.
o Children who have an IV catheter, or are likely to need one placed because of critical
illness, should receive systemic glucocorticoids intravenously.
o Oral dexamethasone phosphate is an alternative for children who vomit oral prednisolone
(dose: 0.6 mg/kg; max 16 mg).
• No CXR or tests in ER
• No Antibiotics in ER & avoid IV lines if possible
Wheezing (1st/recurrent) but NOT severe

• Nebulized salbutamol up to 3 times in l hr; document response
• Steroids for recurrent wheezers
• No initial CXR, CBC, or antibiotics
• Possible complications? call pediatric resident
• Most small babies with bronchiolitis will be admitted
CXRs for wheezers

• Try to hold CXRs until after 6 hours of treatment
• If no response, then consider CXR if any suspicion of complication
• Clinical judgment may need CXR sooner, but NOT before treatment of wheezing!
225
CBCs for wheezers
• Hold CBCs at least until 6 hours after arrival
• If no response, then consider CBC if suspicion of secondary infection
Antibiotics for wheezers

• Only after clear indications
• None, if no fever
• Do not interpret bronchial mucus as alveolar crepitations
• Yes, if AOM, bacterial sinusitis, or other bacterial infection (such as typhoid)
• Yes, if consolidation
ER Steroids for wheezers

• No, if 1st time wheezing & <2 y age
• Yes, if recurrent wheezing
• Yes, if on any steroid now
• Yes, if on steroids in last 3 to 6 months
Advanced treatment for severe wheezing

• Ipratropium bromide nebulization (< 12 years: 250mcg, ≥12 years: 500 mcg). Can be given every
20 minutes for 3 doses followed by PRN.
• May need SC adrenaline (1:1000 solution: 0.01mg/kg SC)
• If no improvement call PICU on call
• Magnesium sulfate only in the ward if unresponsive to above treatment. Dose: 25 – 50 mg/kg IV
slow over 10-20 minutes (max 2 grams)
• For those who fail to respond to above
o Terbutaline (10 microgram/kg IV loading dose administered over 10 minutes, followed by an
infusion of 0.1 to 0.4 microgram/kg per minute), and/or
o Aminophylline and no history of administration of theophylline in the past 24 hours (6 mg/kg
IV loading dose, followed by infusion of 0.6 to 1.5 mg/kg per hour)
• Antibiotics (if clear indications), hydration, chest physical therapy, mucolytics, or sedation.
Discharge from ER
For recurrent or non-severe cases:
• If the child responds well to a trial of bronchodilator treatment (salbutamol nebulization)
• If there are no signs of respiratory distress off 02, can be discharge on:
o Salbutamol (inhaler with spacer) 1-2 puffs 4-6 hourly as and when needed, and Prednisolone
1 mg/kg/day for 3-5 days (if given in ER)
226
2. STRIDOR
Differentiating CROUP from EPIGLOTTITIS

Croup Epiglottitis
Etiology Mostly Parainfluenza virus Haemophilus influenzae B
Onset Over days Over hours

Preceding coryza Yes No
Cough Severe, barking Absent or slight
Able to drink Yes No
Drooling No Yes
Appearance Unwell Toxic and ill
Fever <38.5° C (101.3° F) >38.5° C (101.3° F)
Stridor Harsh, rasping Soft
Voice Hoarse Reluctant to speak, muffled
Wheeze Often present Absent
Position Irritable, active Sitting forward, neck extended
Management of acute epiglottitis

• Call for help from pediatric, anesthetist and ENT teams if required
• Do not do anything else unless the patient obstructs his/her airway
• Keep the child calm and reassure; do not upset with blood tests, CXRs etc
• Do not examine the throat
• Nurse upright
• If the patient obstructs his/her airway, the child needs ET intubattion, which can be difficult to
perform. Go for cricothyroidotomy if ET intubation cannot be performed (Get help from ENT and
anaesthetic teams)
• Definitive management will include intubation by an anaesthetist, blood culture and epiglottis
swabs, intravenous antibiotics, and chemoprophylaxis for household contacts
Management of croup
• Admit if there is stridor at rest
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• Keep calm. That includes the child, carers, nurses, and doctors
• Nurse in a warm, humidified room, & in an upright position. Keep hydrated.
• Treatment:
o For children with moderate stridor at rest and moderate retractions,

dexamethasone (0.15mg/kg is as effective as 0.3 mg/kg or 0.6 mg/kg, maximum of 10 mg)
by the least invasive route possible: oral if oral intake is tolerated, intravenous if IV access
has been established, IM if oral intake is not tolerated and IV access has not been established.
If severe symptoms, higher dose of 0.6mg/k is preferred. Patan Hospiotal has 0.5 mg
dexamethasone tablets. Small infants may not like this tablet form. The intravenous
preparation (4 mg per mL) can be given orally.
o For children with moderate stridor at rest and moderate retractions, or more severe
symptoms, nebulized epinephrine should be given in addition to dexamethasone:
o L-epinephrine is administered as 0.5 mL/kg per dose (maximum of 5 mL) of a 1:1000
dilution. It is given via nebulizer over 15 minutes.
o Nebulized epinephrine can be repeated every 15 to 20 minutes. The administration of three
or more doses within a two- to three-hour time period should prompt initiation of close
cardiac monitoring if this is not already underway.
o Oxygen should be instituted in children with clinical evidence of hypoxia. Do not rely on
oxygen saturations. Humidify the oxygen.
o Intubation is the last resort and is indicated if there is hypoxia with progressive airway
obstruction, fatigue, or worsening hypoxia.
• Where to monitor? Admission to PICU is indicated if there is hypoxia, the child is ill enough
to require nebulised adrenaline, or if it looks like intubation will be necessary.
• What does not help? Steam inhalation, antibiotics, sedation, blood tests, X-rays.
Differential diagnosis of upper airway obstruction

Croup (laryngotracheobronchitis), Bacterial tracheitis, Acute epiglottitis, Laryngeal foreign body,
Diphtheria, Retropharyngeal abscess, Angioneurotic oedema, Laryngomalacia
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3. BRONCHIAL ASTHMA
Management of acute severe asthma
• High flow oxygen

• Salbutamol nebulization x 3
• Ipratropium ( <20 kg: 250 mcg/dose; >20 kg or >6 yrs 500 mcg)
if no improvement with first dose of salbutamol
• Steroids (IV only if not able to take/tolerate orally)
No improvement Improves
• Consider admission
• Continue steroids and salbutamol nebulization as indicated
• Continue ipratropium 6 hourly if it has already been given
Improves
• Admit to children ward

• Continue oxygen, steroids and salbutamol nebulizations
• Also continue ipratropium 6 hourly
No improvement
• Give adrenaline SC if no improvement
No improvement
• Admit to PICU
• Magnesium sulphate IV (25 - 50mg/kg; max 2 gm)
• If no improvement, Aminophyllin IV(6 mg/kg loading followed by infusion of 0.6 – 1.5
mg/kg/hour)
• Consider intubation if no improvement
Indications for intubation

• Hypoxemia despite provision of high concentrations of oxygen
• Severe and unremitting work of breathing (eg, inability to speak)
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• Altered mental status
• Respiratory or cardiac arrest
Judging the severity of asthma

Mild / Moderate Severe Life threatening
Altered level of consciousness Nil Evolving Yes
Exhaustion Nil Evolving Yes
Cyanosis Nil Evolving Yes

Wheezy + + silent Chest
Retraction Absent/mild Present Obvious
Accessory muscle use Absent Present Obvious
Initial PEFR (% predicated or usual) >50-60 <50 <33
SaO2 <92%
4. TRAUMA
Prioritizing in trauma
A = Clear airway, protect C-spine BEFORE assessing and treating the patient
B = Assess and treat breathing
C = Assess and treat hemorrhage, which may require laparotomy/ thoracotomy to control
D = Asses and treat minor and/or extremity injury
D = Assess AVPU
After ABCDE satisfactory and stable

• Complete head to toe examination, including front and back
• Complete X-rays
• Complete investigations
• Reassess ABCD
• Transfer or refer for definitive care
If there is any deterioration at any stage reassess ABCDE
Initial assessment and management
Airway with cervical spine control

Is the airway clear? i.e. speaking or crying. If so give high flow oxygen. If the airway is
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not clear give high flow oxygen and perform the following sequential maneuvers to clear
it:
• Chin lift, jaw thrust (do not tilt head - may have cervical spine fracture!)
• Rigid suction
• Oropharyngeal airway (measure from the incisor teeth to angle of jaw - do not use if it
makes the child gag)
• Intubation by the most experienced person available
• Needle cricothyroidotomy may be necessary
• Immobilise the neck with
o Hard collar
o Blanket roll or sandbags or fluid bags
o Tape across head and collar onto a spinal board
• If combative, use a hard collar only
Breathing
Once the airway is clear and the C-spine is immobilized, see if breathing is present and
adequate? - if not, ventilate using a bag-valve-mask system connected to high flow oxygen,
using a tight-fitting face mask - this works best with one person holding the mask and one
squeezing the bag. Intubation may be required. See if trachea is central. Auscultate in both
axillae to see if there is significant difference in air exchange. Count the respiratory rate.
Assess the work of breathing – nasal flare, head nodding, subcostal/intercostals/suprasternal
recession? Check if there are wounds, marks or fractures. If tension pneumothorax is suspected
clinically do a needle thoracentesis followed by chest drain - do not wait for chest X-ray.
Circulation and hemorrhage control

• Stop obvious external hemorrhage with direct pressure and elevation if possible
• Insert two or more large bore IV cannulae and draw blood for CBC, cross-match, glucose
and urea and electrolytes, and amylase if required.
• Take a set of arterial blood gases
• Look for features of shock – tachycardia, hypotension, delayed CRT (>3sec in neonate,
>2sec in older child)
• If in shock, replace fluid as follows:
NS 20ml/kg bolus
Reassess; if still in shock
NS 20 ml/kg bolus
Reassess; if still in shock

Blood 10 ml/kg and contact surgical team
• If you cannot establish IV access, get intraosseous access or perform a saphenous cutdown.
Avoid attempting central venous cannulation in shocked children.
• If the patient is shocked & intoxicated, has reduced conciousness, or is otherwise
difficult to assess he or she should have intra-abdominal haemorrhage excluded.
Diagnostic peritoneal lavage should be performed by the surgeon who will perform any
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necessary operation.
Disability (neurological status)

• Rapid assessment
oA– Alert
oV– Responds to verbal stimuli
oP– Responds to painful stimuli
oU– Unresponsive
• Pupils
• Children's coma scale
Exposure
Completely undress the child but cover with blanket as all necessary procedures and
examination are completed.
X-rays
• Lateral cervical spine (pull arms gently so C7/T1 can be seen)
• Chest X-ray
• Pelvis X-ray
Nasogastric tube
Gastric dilation is very common in traumatized children. Pass orally if you are worried about
basal skull fracture.
Urinary catheter
Urinary catheter is required if the child is unconscious or shocked or has an abdominal injury.
Do not attempt if you suspect urethral injury.
Analgesia
Severe pain should be relieved as soon as possible. The presence of a head injury is not an
absolute contraindication provided airway and breathing are closely monitored. Intravenous
morphine is the drug of choice( 0.1 mg/kg in an infant or 0.2 mg/kg in the older child).
Give the calculated dose in small increments until the pain is relieved. Never give morphine
IM in trauma. Always record the time and dose given. The effects can be reversed rapidly
with naloxone if required. Femoral nerve block can be used for shaft of femur fractures.
Tetanus Immunization may be required.
Arterial blood gases: All patients with breathing problems should have ABGs measured as
early as possible and repeated if there is any change in clinical
5. STATUS EPILEPTICUS
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Time (min) Intervention
0–5 Stabilize the patient
Assess airway, breathing, circulation, and vital signs
Administer oxygen. Obtain intravenous or intraosseous access
Correct hypoglycemia if present (dextrose 10% @ 5 mL/kg)
Obtain laboratory studies: Glucose, electrolytes, calcium, magnesium, BUN,
creatinine, and LFTs, CBC, blood culture (if infection is suspected)
Initial screening history and physical examination
5–15 Lorazepam, 0.05–0.1 mg/kg IV over 2-5 minutes every 5-10 minutes if
required (max: 4mg/dose)
Diazepam, 6 months-5years: 0.2–0.5 mg IV (0.5 mg/kg rectally) up to 5mg,
> 5 years: 5-10mg IV every 5-10 minutes (maximum 30 mg). May be
repeated 2-4 hours later PRN
15–35 If seizure persists, load with

Phenytoin15–20 mg/kg IV slowly, or
Phenobarbitone 15–20 mg/kg IV slowly (not to exceed 2mg/kg/min)
45 If seizure persists:
Load with phenobarbitone if phenytoin was previously used
Additional phenobarbitone 5 mg/kg/dose every 15–30 min (maximum total
dose 30 mg/kg; be prepared to support airway and breathing)
Between doses of phenobarbitone, paraldehyde (0.4 ml/kg rectally in an

equal volume of cocconut oil or as a 10% enema in normal saline) may be
used
60 If seizure persists, consider midazolam continuous infusion or general anesthesia in
ICU
If seizure was controlled with diazepam or lorazepam, a loading dose of phenytoin
should be given to maintain effect and a maintenance dose of 5 mg/kg/day IV divided
into two equal doses daily is begun 12 hr later
This maintenance dose should also be given to those who were controlled with
phenytoin
If phenobarbitone controlls the seizure, a maintenance dose of 5 mg/kg of

phenobarbitone divided into two equal doses daily is begun 12 hr later
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6. COMA
Coma is a state of ‘unarousable unresponsiveness’.
Children's coma scale

Sign GCS Paediatric GCS Score
Spontaneous Spontaneous 4
Eye To command To sound 3
opening To pain To pain 2
None none 1
Oriented Age-appropriate vocalization, smile, or orientation
to sound, interacts (coos, babbles), follows objects 5
Confused, disoriented Cries, irritable 4
Verbal Inappropriate words Cries to pain 3
response Incomprehensible Moans to pain 2
sounds
None None 1
Obeys commands Spontaneous movements (obeys verbal command) 6
Localizes pain Withdraws to touch (localizes pain) 5
Withdraws Withdraws to pain 4
Abnormal flexion to Abnormal flexion to pain (decorticate posture) 3
Motor pain
response Abnormal extension to Abnormal extension to pain (decerebrate posture) 2
pain
None None 1
BEST TOTAL SCORE 15
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Some causes of coma in children
• Infections: Bacterial meningitis, viral encephalitis, post infectious encephalomyelitis, syphilis,
sepsis, typhoid fever, malaria.
• Hypoxic: Ischemic brain injury following respiratory or circulatory failure, near-drowning.
• Epileptic seizures
• Trauma: Intracranial hemorrhage, cerebral edema or contusion.
• Poisons: Lead, thallium, mushrooms, cyanide, methanol, ethylene glycol, carbon
monoxide.
• Drugs: Sedatives, barbiturates, other hypnotics, tranquilizers, bromides, alcohol, opiates,
paraldehyde, salicylate, psychotropics, anticholinergics, amphetamines, lithium,
phencyclidines, monoamine oxidase inhibitors.
• Metabolic: Renal or hepatic failure, Reye's syndrome, hypoglycemia, diabetic acidosis,
hypothermia, Addison's disease, Acute hypo- or hypernatraemia, rare childhood
metabolic disorders.
• Hypertension
• Vascular or space occupying lesions
Evaluation:
General examination:
• Temperature, heart rate, respiration, blood pressure, skin
• Fundoscopy
• Meningismus
Neurologic examination:
• Level of consciousness
• Motor responses
• Brain stem reflexes
• Pupils
• Eye movement
Screening tests
• CBC, Blood glucose, electrolytes, Urea, creatinine, LFTs, Blood culture
• Urine analysis
• Urine for toxicology where appropriate
• CT scan of head (do emergently if focal neurological signs or papilledema is present)
• Lumbar puncture (do emergently after ensuring absence of papilledema or other signs of raised ICP,
if fever, high white cell count and meningismus)
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• Other laboratory tests: Coagulation profile, metabolic screening, drug concentrations if indicated
• EEG if non-convulsive seizure is suspected
Management:
• ABC
o Intubate if GCS is ≤ 8or respiratory failure
o Cervical spine stabilization (if there is history of trauma)
o Oxygen
o IV access
o Blood pressure support as indicated
• Dextrose: 10% Dextrose 5ml/kg iv after drawing blood (Do NOT wait for the results to give
dextrose)
• Treat definite seizures:
o Lorazepam: 0.1 mg/kg iv (max single dose 5 mg) or
o Diazepam: 6 months to 5 years: 0.2-0.5 mg IV, > 5 years 5-10 mgIV
(Can also be given PR: 2-5 years: 0.5 mg/kg, 6-11 years: 0.3 mg/kg, ≥ 0.2mg/kg)
Emperic treatments:
• For possible infection
o Ceftriaxone (100 mg/kg IV, maximum single dose 2 g), Vancomycin (age specific dose), and
Acyclovir (age specific dose)
• For possible ingestion
o Naloxone: (If opiate intoxication is suspected: miosis, repiratory dipression, hypotonia): <20
kg: 0.1 mg/kg IV, IM, SC, or ET (maximum dose, 2 mg), >20 Kg or > 5 years: 2 mg IV, IM,
SC or ET. Repeat as necessary, keeping in mind its short half life
• For possible increased ICP
o Mannitol: 0.5 to 1 gram/kg IV
• For possible non-convulsive status
o Lorazepam: 0.1 mg/kg IV (max single dose 5 mg) or
o Diazepam: 6 months to 5 years: 0.2-0.5 mg IV, > 5 years 5-10 mg IV
(Can also be given PR: 2-5 years: 0.5 mg/kg, 6-11 years: 0.3 mg/kg, ≥ 0.2mg/kg)
If suspicion of seizures continue, treat as status epilepticus
• For possible Wernicke encephalopathy
o Thiamin: 100 mg IV (before starting glucose). Consider in adolescents for deficiencies
secondary to alcoholism or eating disorders.
• If ingestion of toxic substances is suspected, airway must be protected before GI
decontamination
• Monitor Glasgow Coma Scale and reassess frequently
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7. NEUROCYSTICERCOSIS
Differential diagnosis:
• Brain abscess
• Cerebral amebiasis
• Central nervous system (CNS) tumors
• CNS toxoplasmosis
• Mycotic granulomas
• Neurosarcoidosis
• Tuberculosis of the CNS
• Carotid disease and stroke
General considerations:
• Administer antiepleptic therapy to all patients with seizure
• Always give steroids if antiparasitic treatment is admininstered
• If cerebral edema is present, treat cerebral edema before administering antiparasitic treatment
Treatment of parenchymal NCC
• Antiepileptic therapy: Phenytoin or Carbamazepine (monotherapy is usually sufficient)
o Administered to all patients with NCC who present with seizures or
o If seizure is absent but multiple lesions are seen in the CT scan, specially degenerating lesions
and those with surrounding inflammation
o Continue for 6-12 months after radiographic resolution of active parasitic infection
o If the patient has recurrence of seizure during trial off of antiepileptic treatment, long-term
treatment should be re-instituted
• Antiparasitic therapy: Consider in all patients with NCC and always use together with
corticosteroids
o Single lesion:
 Albendazole: 15 mg/kg/day for 7 days
 Prednisolone: 1 mg/kg/day for 5-10 days
Or Dexamethasone 0.1 mg/kg/day for 5-10 days followed rapid taper
o Multiple lesion:
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 Albendazole: 15 mg/kg/day in two divided doses for 10-15 days
 Dexamethasone high dose
**For subarachnoid disease, Albendazole should be given for 28 days**
• Anti-inflamatory therapy: Indications for corticosteroids
o Along with antiparasitic therapy
o Cysticercal encephalitis
o Subarachnoid cystecercosis
Things to do before initiating corticosteroids
o Mantoux test (and other investigations as indicated) to rule out tuberculosis
o If indicated, screen for strongyloidiasis
o Ophthalmologic examination to rule out ocular cystecercosis
Indications for surgical intervention
• Altered mental status or impaired herniation due to hydrocephalus secondary to NCC
• Intraventricular cysts with hydrocephalus
• Subarachnoid cysticercosis (giant cysticerci)
• Ocular cysticercosis
• Spinal cysticercosis
Follow-up
• CT scan
o In 1-2 months and then after 6 months of diagnosis of parenchymal or subarachnoid

cysticercosis. Once lesions have resolved, imaging is less useful.
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o Before discontinuing antiepileptic drugs
o New, worsening or persistent symptoms
• Patients with VP shunts should be educated to seek prompt medical advice for symptoms of
hydrocephalus
8. DRUG/ FLUID DELIVERY IN A SICK CHILD

Intravenous access:
If cannot be established within 90 seconds, go direct to intra-osseous access!
• In children any IV access anywhere is effective if drugs are flushed through after
administration.
• Central venous access is the best route of administration; but should only be attempted
by experienced personnel and is relatively contraindicated in trauma patients.
Intraosseous access:
• After giving drugs, flush them through. Dilute strong alkalis and hypertonic solutions.
Setting up intraosseous infusion

Equipment:
Alcohol or Betadine swabs:
Intraosseous needle or 16-gauge cannula at least 1.5 cm in length
20 ml syringe with normal saline
Infusion fluid
Procedure:
Identify the infusion site. Avoid fractured bones, or limbs with proximal fractures. If possible
avoid areas of infected burns or cellulitis.
Proximal tibia: Anteromedial surface, 2-3 cm below the tibial tuberosity.
Distal tibia: Proximal to the medial malleolus.
Distal femur: Midline, 2-3 cm above the external condyles.
• Prepare the skin and if necessary use local anesthetic.
• Insert the needle through the skin, perpendicularly and slightly away from the growth plate
239
into the bone with a screwing motion. There is a feeling of ‘giveway’ as the marrow cavity
is entered. Unscrew the trocar and confirm position by aspirating bone marrow or by
flushing with 5-10 ml normal saline.
• Secure the needle and splint the limb.
Fluids can be infused through an intraosseous needle as through a standard intravenous

cannula. If rapid fluid replacement is required, infuse under pressure using a 50 ml syringe.
Dilute strong alkalis and hypertonic solutions.
After giving any drug- flush it through.
Contraindications: Ipsilateral fracture, ipsilateral vascular injury, osteogenesis imperfect,

osteoporosis.
Complications: Failure to enter the bone marrow, extravasation or sub-periosteal infusion.

Osteomyelitis is rare with short term use. Local infection, skin necrosis, pain, compartment
syndrome; fat and bone marrow microemboli have all been reported.
Doses of pharmacologic agents in pediatric resuscitation

Oxygen 100% initial dose, wean as clinically indicated
Glucose Newborns: 10% Dextrose 2ml/kg IV
Children: 10% Dextrose 5 ml/kg IV
Epinephrine 0.01 mg/kg IV/IO (0.1 mL/kg of the 1:10,000
solution). Repeat every 3-5 min as required
0.1 mg/kg endotracheal (ET) (0.1 mL/kg of
the 1:1000 solution)
Atropine 0.02 mg/kg IV or IO (minimum 0.1 mg,
maximum single dose 0.4mg)
Sodium bicarbonate 1meq/kg IV/IO initial dose over 1-2 minutes,
then
0.5 mEq/kg subsequent doses every 10
minutes of arrest. Maximum 8 meq/kg/day
Endotracheal tube sizes

Rough guide: Tube diameter = Diameter of child's little finger
or nostril
Internal diameter (mm) = (Age/4) + 4 in a child over one year
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Length (cm) = (Age /2) + 12 for an oral tube
Length (cm) = (Age/2) + 15 for a nasal tube
9. INITIAL ASSESSMENT OF A SICK CHILD
Airway and Breathing:

Obstruction?
Work of breathing - grunting, nasal flaring, recession or in drawing
Respiratory rate
Auscultation
Cyanosis?
Circulation:
Heart rate
Pulse volume
Capillary refill
Skin temperature
Disability:
Posture and tone
Pupils
Mental status - the AVPU scale
A - Alert
V - Responds to verbal stimuli
P - Responds to painful stimuli
U - Unresponsive
It should be possible to perform this assessment within the first minute. If the child is very sick,
CALL FOR HELP. It is better to call for help early. You can then go on to:
Initial management
Initial formal observations: pulse, respiration, BP, temperature, O2 saturations, BM stix, weight
Initial investigations
Definitive management
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10. BASIC LIFE SUPPORT (AHA GUIDELINE, 2013)
Component Recommendations
Children Infants
Recognition Unresponsive
No breathing or only gasping
No pulse felt within 10 seconds
CPR sequence Chest compressions, Airway, Breathing (CAB)
Compression rate At least 100/min
Compression depth At least 1/3 AP diameter At least 1/3 AP diameter
About 2 inches (5 am) About 1 ½ inches (4 cm)
Chest wall recoil Allow complete recoil between compressions
Attempt to limit interruptions to <10seconds
Compression interruptions Minimize interruptions in chest compressions
Attempt to limit interruptions to <10 seconds
Airway Head tilt-chin lift (suspected trauma: jaw thrust)
Compression-ventilation 30:2 (Single rescuer)
ratio (until advanced 15:2 (2 rescuers)
airway placed)
Ventilation with advanced 1 breath every 6-8 seconds (8-10 breaths/min)
airway Asynchronous with chest compressions
About 1 second per breath
Visible chest rise
Defibrillation Attach and use AED as soon as available.
Minimize interruptions in chest compressions before and after shock;
Resume CPR beginning with chest compressions immediately after each shock
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11. BURNS
Don't panic when faced with a burned child. Adhere to the basic principles of resuscitation
Burns: Calculating percentage body surface area
Child's own adducted fingers and palm is approx 1% of or her body surface area. Use the
chart below to estimate the surface area involved.
Complete a burns chart while examining the patient. (Remember to examine the patient's back
and back of the limbs.)
% OF TOTAL BODY SURFACE AREA AT:

Area Newborn 1 year 5 years 10 years 15 years
indicate
A 9-5 8-5 6-5 5-5 4-5
B 2-75 3-25 4 4-5 4-5
C 2-5 2-5 2-75 3 3-25
Definition of severe burn:

• ≥ 25% total body surface area (TBSA) burn in ≥10 year olds (exclude superficial burn)
• ≥ 20% TBSA burn in <10 year olds
• ≥ 10% full thickness burn
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• All burns involving eyes, ears, face, hands, feet, or perineum that are likely to result in
cosmetic or functional impairment
• All high-voltage electrical burns
• All burn injuries complicated by major trauma or inhalation injury
• All patients with burn injuries and serious co-morbidities
Emergency management:
Airway and cervical spine
The airway is in danger if.
• Burns to face, mouth, or neck
• Any suspicion of inhalation injury
• Severe smoke exposure in confined space
• Soot in mouth or nose
• Soot in sputum
• Wheeze or stridor
o Any of the above should warn that intubation and ventilation maybe required. CALL FOR
HELP URGENTLY. The child may deteriorate rapidly so do not delay intubation if the
airway is at risk.
o Immobilize the cervical spine if injury is suspected.
Breathing
All patients should be given high flow oxygen. If breathing is absent or inadequate the child
will need intubation and ventilation.
Circulation
Presence of shock immediately after burn is due to other injuries. IV access should be
obtained rapidly, preferably through non-burned skin (but you may have no other
option).
Use the intraosseous route if intravenous access cannot be obtained.
Take blood for Hb, urea and electrolytes, and cross matching. Take a set of arterial blood gases
and request carboxyhaemoglobin.
Give 20ml/kg crystalloid bolus initially.
Disability
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Reduced consciousness level is due to hypoxia, hypovolaemia, and head injury until
each is excluded sequentially.
Exposure
Get all clothing off to examine and then cover as soon as possible due to risk of hypothermia
during assessment.
Assessing burn injury:

Depth
Superficial
• Erythema only
• No blisters
• Do not count in % burn
Partial thickness
• Usually blistered
• Skin pink or mottled
Full thickness
• Skin white or charred
• Painless
• Leathery, dry to touch
Treatment:
• Analgesia: Severe pain should be treated with intravenous Morphine Dose: 0.1 mg/kg iv in
an infant or 0.2 rng/kg iv in a child. Continuous infusion @0.02 to 2.6mg/kg/hr iv (average
0.06mg/kg/hr) can be given.
• Fluid:
• Therapy for shock if indicated (20 ml/kg crystalloid or colloid)
• Normal maintenance fluids
• If burns >10% the child will require additional fluids (usually 4% albumin) which can be
estimated according to the Parkland’s formula.
Parkland’s formula:
245
Percentage burn x Weight (in kg) x 4 (in ml)
Half of this should be given in the first 8 hours since the time of the burn. The rest will be
given over the next 16 hours.
• Thromboembolic event prophylaxis:

o Enoxaparin or Heparin (if renal impairment)
• Other
o Cool burns with soaks or irrigation (not if >10% and not longer than 5-10 minutes).
Once the wounds are cooled, dress with paraffin gauze or clingfilm (not flamazine).
o Insert a urinary catheter if a major burn - aim for at least 1 ml/kg/hour urine output.
o Insert NG tube for gastric decompression.
o Burns require tetanus cover.
o Discuss with burns unit fully and if necessary transfer.
12. CHOKING
Open
airway Breathe
Check 5 back
Mouth blows
5 Chest
thrusts
2nd time around
in children over 1
year
5
abdominal
thrusts
Do not perform blind finger sweeps. Back blows are delivered between the shoulder blades.
The child's head should be lower than the abdomen.
246
Chest thrusts are similar to chest compressions except they are sharper and more vigorous.
They should be performed at a rate of one every 3 seconds.
Abdominal thrusts can be performed in children over a year of age. Use the Heimlich
manoeuvre in conscious children or lay the unconscious child supine. Direct the thrusts
upwards towards the diaphragm.
CONTINUE THE CIRCUITS UNTIL THE FOREIGN BODY IS CLEARED.
13. NUTRITION REQUIREMENTS FOR CHILDREN
Adapted from "Dietary Reference Values for Paediatrics",

The Hospitals for Sick Children, London, 1992.
Normal requirements High requirements
Energy Protein Energy Protein
4-12 95 kcals/kg/d 1.5 g/kg/d 130-150 3-4.5 g/kg/d
mont kcals/kg/d
hs
1-4 95 kcals/kg/d 1.1 g/kg/d 120-150% 2 g/kg/d
years normal require.
4-6 85 kcals/kg/d
years
Suggested use of Paustik Sanjivvani (as nutrition supplement):

Children aged 5 - 1 0 years, 500 ml/day
Children aged >10 years, 1000 ml/day
Special milk': i n i t i a l feed for severely malnourished children >6 months 130 ml/kg/day (=99
kcals, 1.4 g. protein, /kg/day) divided as 3 hourly feeds
Ward Food Values

Energy Proteing
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Kcals G
Tea ( Sugar – free) 80 (40) 2
Haluwaa 264 5
Sugar – Free Porridge 249 11
Milk 120ml 80 4
Yoghurt 120ml (140g) 84 4
Lito : full 150 ml 209 6
Half 75 ml 105 3
Khichiri 359 11
Rice meal : full 807 19
Half 505 12
Quarter 296 8
Afternoon Snack : full 436 11
Half 286 8
Quarter 244 6
Special milk 100ml 76 1
Paustik Sanjiwani : 500ml 754 27
Sugar free 634
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14. IV FLUID RESCUSITATION IN DEHYDRATION
Laboratory investigations
Serum sodium
• Hyponatraemia (serum Na <130mEq/L)
• Isonatraemia (serum Na 130-150mEq/L)
• Hypernatraemia (serum Na >150mEq/L)
Serum potassium
Both hypokalaemia or hyperkalaemia can occur in dehydration. If the child has
oligurea or anuria, do not add potassium in the iv fluid until serum potassium is
249
determined.
Serum bicarbonate (can be measured by capillary or venous blood gas)
Serum bicarbonate <17 mEq/L almost always suggests moderate to severe dehydration
Serum urea and creatinine may be warranted to assess renal function in cases of
severe dehydration
Calculate deficit and maintenance requirements:

• Maintenance of water = 100/50/20 rule
100cc/kg/day for 1st 10 kg, 50/kg for the 2nd 10 kg, 20/kg rest
• Deficit of water = wet weight x percent dehydration x 10
• Maintenance of Na (sodium) = 3-4 mEq/kg/day

• Deficit of Na =110 to 120 mEq Na loss/L of H2 0 loss
if Hyponatraemia:
Sodium deficit = (135 - measured sodium) X weight X 0.6
Initial treatment for children in hypovolumic shock

What fluid? 0.9% Saline
How much? 20ml/kg Re-assess and repeat as necessary until adequate
perfusion is restored
What route? Preferably by intravenous route. If IV access cannot be
obtained, use intraosseous route without delay
How fast? Rapid infusion
Follow-on fluid management: Depends upon degree of dehydration as well as serum

sodium and potassium values.
Example #1: isotonic dehydration (sick 2 days)

Pre-illness weight 10kg, but on admission 9 kg (therefore 10% dry)
H 2O Na
Deficit 1000 cc 110-120 (serum sodium normal)
250
Maintenance +1000 cc +40 (4mEq/kg X 10kg = 40 mEq)
Total 2000 cc 150-160 mEq
Initial Tx -400 cc in 1 hour - 62 (62 mEq Na in 400 cc NS)
Rest 1600 cc - 88-98 mEq ( 8 8 - 9 8 / 1 . 6L = 55-61 mEq/L
= 28-30/500cc) >1/3 & <1/2 NS
ORDERS : 1. NaCI or Ringer's lactate 400 cc in 1 hour
then, 2. 5% Dextrose in 0.45% NaCI + 5cc KCI/500 cc-- 500 cc
every 8 hours X 3
Example #2: HYPONATREMIC dehydration (sick 3 days)

-pre-illness weight 6.0 kg, but on admission 5.5 kg (therefore -8% dry)
-serum sodium is 119 mEq (135-119 X 6.0kg X 0.7 = 67 mEq added deficit)
H2 O Na
Deficit 500 cc 50 +67 =117 (use 100 Na/L H2O loss
Maintenance + 600 cc +24
Total 1100 cc 141 mEg
Initial Tx -250 cc in 1hors - 39
Rest 850 cc 102mEq (102/85 L= 120 /l = 60/500cc)
1/2NS=37.5mEq/500cc, so need 22 mEq more/bottle
ORDERS 1. NaCI or Ringer's lactate 250 cc in 1 hour

then, 2. Dext 1/2 NaCI + 20 cc NaHCO3 (max 3mEq/kg/12 hours is safe)
+ 5cc KCI/500 cc bottle - one bottle every 14 hours X 2
Example #3: HYPERNATREMIC dehydration

• RESTORE INTRAVASCULAR VOLUME
NS 20ml/kg IV over 20 min if circulation is poor. Repeat until intravascular volume
is restored.
• DETERMINE TIME FOR CORRECTION BASED ON INITIAL SODIUM
CONCENTRATION
251
145-157 mEq/L = 24hr
158-170 mEq/L = 48hr
171-183 mEq/L = 72hr
184-196 mEq/L = 84hr
• ADMINISTER FLUID AT CONSTANT RATE OVER TIME FOR CORRECTION
Typical fluid: D51/2 NS with 5mlKCl/500ml IVF unless contraindicated(No urine output).
Typical rate: 1.25-1.5 times maintenance
HYPOKALEMIA
K <3.5
If serum K+ level = 2.5 to 3.5 -> Do ECG
If ECG normal -> Inc maintenance K oral/iv 3-4 meq/kg/day
If ECG abnormal or symptomatic ->K rapid correction to be given.
If serum K+ <2.5  Get ECG done
Give K rapid correction as follows, 0.3meq/kg/hr.
Stock solution (90 ml NS + 10 cc Kcl)- 0.5ml/kg/hr, under ECG monitor & increase maintenance
dose
K+ to 3-4 meq/kg /day. K rapid correction can be repeated as necessary.
1 Abnormal ECG—flat T waves, U waves depressed ST segment, arrhythmia
2 Symptomatic—paralytic ileus, muscular weakness.
15. URINARY TRACT INFECTION

Any newborn over 72hrs of age with fever should have a urine culture taken as part of the septic
screen. This can be collected by catheterisation, suprapubic aspiration or in older children by a
clean void.
Criteria for diagnosis are as follows:
Method Colony count (pure culture)
Suprapubic aspiration any gram negative organism is positive, more than a few
thousand gram positive organisms is positive
Catheterized specimen >100,000 organisms infection likely
< 10,000 unlikely, repeat culture.
Clean Void Boy- > 10,000 infection likely
Girl- > 100,000 infection likely
252
Antibiotics
• Infants < 2 months: IV antibiotic (<2 months: amikacin , or cefotaxime)
• > 2months: Oral ofloxacin if not vomiting. IV amikacin or ceftriaxone if vomiting
• If enterococcal UTI is suspected or proven: Add Ampicillin
Duration of antibiotics
• Infants <2 months: Continue IV antibiotics for 10 days
• > 2 months and febrile or immunocompromised: If on iv antibiotics, continue IV antibiotics
until afebrile. Change to oral antibiotics once afebrile and continue for a total duration of 10
days
• > 2months and afebrile in immune competent children: Oral antibiotics for 5 days
Repeat urine culture:

• No need to repeat urine culture if the pathogen is susceptible to the antibiotic being used and
the patient is responding as expected
• Repeat urine culture after 48 hours of treatment if the pathogen is not susceptible to the
antibiotic being used or if the patient is not responding to the treatment
Indications for hospitalization:

• Age <2 months
• Clinical urosepsis (eg, toxic appearance, hypotension, poor capillary refill)
• Immunocompromised patient
• Vomiting or inability to tolerate oral medication
• Lack of adequate outpatient follow-up (eg. Lives far)
• Failure to respond to outpatient therapy
ANTIBIOTICS USED FOR UTI PROPHYLAXIS

Indications:
• Grade III VUR
• Recurrent UTI in children without VUR: three febrile UTIs in six months or four total
253
• Consider in children less than 2 months if USG is abnormal till MCUG is done to exclude
renal tract abnormalities (no clear recommendation available at present).
ANTIBIOTIC DOSAGE
Co-trimoxazole 2 mg/kg of trimethoprim HS

Nitrofurantoin 1-2 mg/kg HS
Cephalexin 25mg/kg HS
In pseudomonas UTI, consider 3.75mg/kg HS
Ciprofloxacin
Cefadroxil Under 1 year: 12.5mg/kg HS

1 to 6 years: 125mg HS
• Continue prophylaxis for 6 months. If UTI does not occur during prophylaxis, discontinue
prophylaxis. Re-start if infection recurs after discontinuation of prophylaxis
• If UTI develops while on prophylaxis it should be treated with a different antibiotic and the
prophylactic antibiotic should be changed according to sensitivities.
Always check that the infecting organism is sensitive to what the patient is being treated with.
Indications for renal and bladder USS

• Children younger than two years of age with a first febrile UTI
• Children of any age with recurrent febrile UTIs
• Children of any age with a UTI who have a family history of renal or urologic disease, poor
growth, or hypertension
• Children who do not respond as expected to appropriate antimicrobial therapy
When to perform the USS?

• As soon as possible during the acute phase of illness in patients with unusually severe illness or
those not responding to antimicrobial treatment as expected
• After the acute phase of illness in those who respond to appropriate treatment
Indications for MCUG

• Children of any age with two or more febrile UTIs.
• Children of any age with a first febrile UTI who have a family history of renal or urologic
disease; children with poor growth or hypertension.
• Children with abnormal voiding pattern (dribbling of urine).
• Urinary tract anomalies are more frequent among children with UTI caused by pathogens other
than E. coli
• If the renal and bladder utrasonography reveals hydronephrosis, scarring, or other findings that
suggest either high grade VUR or obstructive uropathy.
• In children less than 2 months if USG of kidney and bladder is abnormal (no recommendations
available at present).
When to perform MCUG?
254
• During the last days of antimicrobial therapy or immediately after completion of the
antimicrobial therapy for UTI (early imaging does not increase the false positive diagnosis of VUR
and helps to avoid use of prophylactic antibiotics in those without VUR)
16. NEPHROTIC SYNDROME

EVALUATION OF CHILDREN WITH SUSPECTED NEPHROTIC SYNDROME
Recommendations for initial evaluation include:
● Urinalysis
● First morning urinary protein /creatinine ratio (normal value for 6 months to 2 years: <0.5 mg
protein/mg creatinine , > 2 years: <0.2 mg protein/mg Creatinine)
-The child should be instructed to void before bed and collect the first morning sample
● Serum electrolytes, serum urea nitrogen, creatinine, and glucose
● Serum cholesterol
● Serum albumin
● *Serum Complement 3 level

● *Antinuclear antibody level* (for children aged >=10 years or with any other signs of systemic
lupus erythematosus);
● *Hepatitis B, hepatitis C, and HIV serology in high-risk populations*
● *Purified protein derivative level* and
*These tests should be sent only after the diagnosis of nephrotic syndrome
- Kidney biopsy should be considered for children aged ≥12 years who are diagnosed with
nephrotic syndrome
Criteria for diagnosis of nephrotic syndrome

• Nephrotic range proteinuria : Urinary protein excretion greater than 50 mg/kg per day or
40mg/m2/hr (measured in 24 hour urine sample) or,
Urinary protein/creatinine ratio >3mg protein/ mg creatine in early morning spot urine sample
• Hypoalbuminemia : Serum albumin < 3 g/dL
Other associated features are

• Edema and
• Hyperlipidemia
DEFINITIONS
The following are terms commonly used for management of nephrotic syndrome.
Remission: Urine protein/creatine <0.2 or dipstix urine albumin negative or trace for 3 days.
Relapse: After remission, an increase in the first morning urine protein/creatinine to ≥2 or urinary
dipstix albumin ≥2 for 3 of 5 consecutive days.
Frequently relapsing: 2 or more relapses within 6 months after initial therapy or >4 relapses in
any 12-month period.
Steroid dependent: Relapse during taper or within 2 weeks of discontinuation of steroid therapy.
Steroid resistant: Inability to induce a remission with 4 weeks of daily steroid therapy.
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Criteria for minimal change disease
• Age older than 1 year and younger than 10 years of age
• None of the following findings: hypertension, gross hematuria, and a marked elevation in serum
creatinine
• Normal complement levels
• No extra-renal symptoms such as malar rash or purpura
Kidney Disease Improving Global Outcomes (KDIGO) 2012 guidelines to manage children
with steroid-sensitive nephrotic syndrome as follows:
Initial therapy:
• Prednisolone 60 mg/m2 or 2 mg/kg per day for four to six weeks (maximum dose of 60 mg/day)
followed by,
• Alternate-day prednisone of 40 mg/m2 or 1.5 mg/kg (maximum dose of 40 mg/day) and
continued for two to five months with tapering of the dose.
Infrequent relapses:
• Prednisone 60 mg/m2 or 2 mg/kg per day (maximum dose of 60 mg/day) until the urine protein
tests are negative or trace for three consecutive days, followed by
• Alternate-day prednisone of 40 mg/m2 or 1.5 mg/kg (maximum dose of 40 mg/day) for at least
four weeks.
Frequent relapses or steroid-dependent disease:

• Prednisone 60 mg/m2 or 2 mg/kg per day (maximum dose of 60 mg/day) until the urine protein
tests are negative or trace for three consecutive days, followed by
• Alternate-day prednisone for at least three months.
• The dose of alternate-day prednisone should be the lowest dose needed to maintain remission
without adverse side effects. In patients in whom alternate-day therapy is not effective in
maintaining remission, the lowest possible dose of daily prednisone is given to maintain
remission to minimize adverse side effects. Daily prednisone should be given to patients during
episodes of upper respiratory tract infection and other infections that are associated with relapse.
• Corticosteroid-sparing agents should be given to children with frequently relapsing or steroid-
dependent disease who develop steroid-related adverse effects. Data are insufficient to choose
among the following agents. Drug selection is based on the reported efficacy, adverse effects,
local availability, and cost.
Corticosteroid sparing agents:

• Cyclophosphamide (dose of 2 mg/kg per day for 8 to 12 weeks [maximum cumulative dose of
168 mg/kg]) or
• Chlorambucil (dose of 0.1 to 0.2 mg/kg per day for 8 weeks [maximum cumulative dose 11.2
mg/kg]).
• Levamisole (dose of 2.5 mg/kg on alternate days for at least 12 months).
• Calcineurin inhibitors include cyclosporine (initial dose of 4 to 5 mg/kg per day given in two
divided doses) or tacrolimus (initial dose of 0.1 mg/kg per day given in two divided doses
256
• Mycophenolate mofetil (initial dose of 1200 mg/m2 per day given in two divided doses for at
least 12 months).
• Rituximab (an anti-CD20 monoclonal) should be considered only in children who have failed
combination therapy of prednisone and other corticosteroid-sparing agents and have serious
adverse effects of therapy.
Both mizoribine and azathioprine are NOT recommended in the management of children with
NS)
Steroid-Resistant Nephrotic Syndrome Management

● Kidney biopsy;
● Tailor therapeutic regimen according to kidney histology; and
● Provide optimal supportive therapy.
Treatment for steroid-resistant nephritic syndrome:
• Immunosuppressive
o Alkylating agents
o Calcineurin inhibitors (CNIs)– Cyclosporin and tacrolimus
o Mycophenolate mofetil
o Rituximab
• Nonimmunologic antiproteinuric therapy
o Angiotensin-converting enzyme inhibitors (ACE-Is)
o Angiotensin receptor blockers (ARBs)
Symptomatic treatment of nephrotic syndrome

• Oedema
o Salt restriction
o Fluid restriction (Insensible loss + urine output)
 Maybe helpful in stabilizing patient’s weight and
 If serum sodium ≤ 130 mEq/L
o Diuretics (Frusemide is the first choice)
Particularly useful when fractional excretion of sodium (FeNa) >2% indication volume
expansion
o Frusemide with albumin
 Anasarca with respiratory compromise due to ascites and/or pleaural effusion
 Severe scrotal oedema
 Peritonitis
 Severe tissue breakdown
• Hypercoagulability: Patients with severe hypoalbuminaemia (serum a albumin <2g/dl) and
fibrinogen level >6g/L are at high risk.
o Mobilisation
o Avoidance of haemoconcentration
o Early treatment of hypovolaemia and sepsis
Prophylactic anticoagulation is not indicated unless there is H/O thromboembolic phenomena
• Infection: Prophylactic antimicrobials are not recommended.
o High risk for development of Pneumococcal or E.Coli infection (Peritonitis, pneumonia,
sepsis)
257
o High risk for varicella infection- treat with Acyclovir if varicella infection develops while
on steroid therapy
**Pneumococcal and varicella vaccines are recommended**
• Hyperlipidaemia: Statins are indicated for only those children who remain persistently
nephrotic and have hyperlipidaemica
• Hypertension: Children with persistent hypertension in nephrotic syndrome are more likely to
develop chronic kidney disease. Therefore, antihypertensive of choice are
o ACE inhibitors or
o Angiotensin II receptor blockers
(Discontinue these drugs if hyperkalaemia cannot be controlled or creatinine clearance is >30%
of the baseline)
• Other dietery measures: No clear role. Low fat diet can be suggested to prevent excessive
weight gain.
17. MANAGEMENT OF DIABETIC KETOACIDOSIS IN

CHILDREN
Diagnostic criteria for diabetic ketoacidosis (DKA)
• Hyperglycemia, serum glucose of >200 mg/dL (11 mmol/L)
AND
• Metabolic acidosis, defined as a venous pH <7.3 and/or plasma bicarbonate <15 mEq/L (15 mmol/L)
Initial assessment
• Neurologic status: GCS ≤7 has poor prognosis
• Acid-base status
• Volume status
• Duration of symptoms
Severity of DKA
efining features Mild Moderate Severe
Venous pH 7.2-7.3 7.1-7.2 <7.1
Serum bicarbonate (mEq/L) 10-15 5-10 <5
Fluid replacement
Deficit assessment: In a patient with moderate to severe DKA, estimate water deficit of 7-
10%
1.Initial volume expansion: In patients with moderate to severe DKS
o 0.9% saline 10ml/kg iv over 1 hour and reassess
o 2nd bolus of 0.9% saline 10ml/kg IV over 1 hour can be given if required
**Do NOT give >20ml/kg of saline bolus unless the patient’s cardiovascular status is
compromised**
Subsequent fluid administration:
258
Type of Fluid:
• For the 4 to 6 hours- Normal saline
• After 6 hours- Change to 0.45% saline provided the sodium concentration is rising as the glucose
concentration decreases, and the patient’s circulatory and mental status are stable.
• If Serum Na < 130 or > 150- Consider continuing with normal saline
• If Serum Na does not increase with treatment- consider continuing with normal saline
• Once Serum glucose decreases to 250- 300 mg/dl - add 5% dextrose
(Hyperglycaemia falsely decreases Serum Na. For each 100mg/dl rise in sugar, serum Na will
decrease by 1.6mg/dl)
• The rate of fluid administration should not exceed 1.5 to 2 times the maintenance rate
• Should not include urinary losses
• The hourly rate of fluid administration should never exceed two times the maintenance rate
(about 3000 ml/m2/day, including the initial bolus) unless there is objective evidence of shock
* Excessive fluids may increase the risk for cerebral edema*
Potassium supplementation: After the initial bolus
Serum Potassium (in mEq/L) Potassium added per Litre of fluid
<3 40-50 mEq/L

3-4 30-40 mEq/L
4-5 20-30 mEq/L
5-6 10-20 mEq/L
Insulin therapy
• Insulin therapy is required to correct metabolic decompensation. Do NOT give sodium

bicarbonate to correct metabolic acidosis in a patient with DKA
• It should start after the first bolus, i.e. from 2nd hour of the treatment
• Too rapid correction of blood sugar can lead to cerebral edema
• Add 50 units of short acting (Regular insulin) to 50 ml of 0.45% saline (1ml=1unit)
o Do NOT give initial bolus of regular insulin
259
o Start with 0.05 to 0.1 units/kg/hour
• Do NOT decrease the rate of infusion of insulin until metabolic acidosis is corrected, even
if the serum glucose is falling
• When the serum glucose concentration decreases to 250 to 300 mg/dL ,change the IV fluid to
5% dextrose in normal saline
• If the serum glucose falls below 250 mg/dL, before complete resolution of the ketoacidosis, the
concentration of dextrose in the IV fluid should be increased to up to 10 to 12.5% Dextrose
(The purpose of adding dextrose to the intravenous solution is to prevent hypoglycemia while
continuing to administer insulin to correct ketoacidosis)
• Desired rate of fall of blood glucose: 50-100 mg/dl/hour.
• The insulin infusion should continue at 0.05 to 0.1 units/kg per hour until the following
conditions are met [9-11]:
o Serum anion gap reduced to normal (12 ± 2 meq/L)
o Venous pH is >7.30 or serum HCO3 is >15 meq/L
o Plasma glucose 100-150in older children, and 150-200 in younger children
o Tolerating oral intake
• Stop IV insulin infusion only after 1 hour of the first dose S/C insulin.
Monitoring:
• Blood glucose: Hourly for the first 4-6 hours of insulin and fluid therapy
• Serum electrolytes and venous pH: Hourly for the first 3-4 hours, then 2-4 hourly as directed by
the results
• Clinical parameters: Heart rate, respiratory rate, blood pressure, oxygen saturation, and
neurologic status should be monitored continuously.
• In patients with severe DKA or altered mental status, frequent neurologic examinations are
recommended.
• Monitor for warning signs and symptoms of cerebral edema including headache,
inappropriate decrease in heart rate, recurrence of vomiting, changes in neurologic status, rising
260
blood pressure, and decreased oxygen saturation
Borderline DKA
• Venous pH >7.30, serum bicarbonate >16 meq/L
• No neurologic impairment
• Estimated volume deficit less than 3 percent
• Not vomiting
These patients may be managed in an ambulatory setting under the supervision of an experienced
medical team. However, hospitalization may appropriate for young children (eg, <5 years of age)
because of their sensitivity to insulin as compared with older children, and because of their
increased risk for cerebral edema. Children of any age should be treated in hospital if the home
environment does not provide close supervision and monitoring.
18. SEPTIC SHOCK

Definition of septic shock:
Septic shock is defined as sepsis with cardiovascular dysfunction that persists despite
administration of >40ml/kg isotonic fluid in one hour.
Cardiovascular dysfunction:
• Hypotension
• Reliance on vasoactive drug administration to maintain a normal blood pressure
Or, two of the following
• Prolonged capillary refill,
• Oliguria,
• Metabolic acidosis, or
• Elevated arterial lactate
Rapid recognition of septic shock:

Inadequate tissue perfusion in a seriously ill child
• Fever
• Tachycardia or bradycardia
• Decreased peripheral pulses compared with central pulses
• Mottled or cool extremities
• “Flash” or >3 second capillary refill
• Dry mucus membranes, sunken eyes, and decreased urine output
• Tachypnea, bradypnea, or apnea
• Hypotension
• Altered mental status (irritability, anxiety, confusion, lethargy, somnolence, apnea)
• Hypothermia (especially neonates)
Signs of infection
Suggestive laboratory findings

• Lactic acidosis (>3.5 mmol/L)
• Age-specific leukocytosis or leukopenia (table 1)
261
• Platelet count <80,000/microL or a decline of 50 percent from highest value recorded over the
past three days
• Disseminated intravascular coagulopathy
• Renal insufficiency suggested by a serum creatinine ≥2 times upper limit of normal for age or
twofold increase in baseline creatinine
• Liver dysfunction implied by a total bilirubin ≥4 mg/dL (not applicable to newborn) or alanine
aminotransferase (ALT) >2 times upper limit of normal for age
262
263
19. RECOGNITION OF MENINGOCOCCAL DISEASE
Figure: Algorithm for the early management of meningococcal infection. (Copyright Pollard AJ, Nadel S, Habxbi P,
Faust I, Maconochie I, Britto Levin M 1998. Department of paediatrics, Imperial College School of Medicine, Si
Mary' Hospital london.) .
Purpuric or petechial rash or signs of meningitis/septicaema
Call consultant in A&E, paediatrics, anaesthetics or intensive care
Shock ?
Raised ICP?
Tachycardia, cold peripheries, increased
Decreasing or fluctuating level of consciousness,
capillary refill time (> 4 s) decreased urine hypertension and relative bradycardia,unequally dilated
output,(<1ml/kg/h) or poorly responsive pupils, focal neurological signs,
tachypnoea/hypoxia seizures, abnormal posture, papilloedema
confusion and decreasing conscious level hypotension
(late sign)
Clinical features of meningitis ?
No
ABC and oxygen (10 l/min) ABC and oxygen (10 l/min) and BM Stix
and Dextrostix, insert 2 large iv cannulae (or Steroids (Dexamethasone, 0.4 mg/kg bd for 2 days)
intra-osseous) Cefotaxime or Ceftriaxone (80 mg/kg)
Cefotaxime/Ceftriaxone Treat shock if present
(80 mg/kg) DO NOT LUMBAR PUNCTURE
Volume
resuscitation
(use 20 ml/kg of colloid as a Give Mannitol (0.25 g/kg) as a bolus
bolus and repeat) [or Frusemide (1 mg/kg) if no urine output)
Observe closely for AND repeat if raised ICP persists
Intubate and ventilate to control PaCO2 (4-4.5 KPa)
Sedate (and muscle relax for transport),
Still shocked ? NG tube
after 40 ml/kg volume replacement 300 Head-up position, midline and avoid neck lines
Dexamethasone
Continue volume resuscitation (boluses of 10-20
(0.4 mg/kg bd
ml/kg of colloid)
for 2 days)
Call anaesthetist and contact PICU
Will need elective intubation and ventilation
Commence inotropes peripherally
Nasogastric tube Cautious fluid resuscitation, but
correct coexisting shock Phenytoin
(18 mg/kg over 30 mins) for
Anticipate and correct: seizures (ECG monitoring) Urinary
raised intracranial pressure catheter (especially after
hypoglycaemia mannitol/frusemide)
acidosis
hypokalaemia
hypocaicaemia Cefotaxime/Ceftriaxone (80
hypomagnesaemia
hypophosphataemia mg/kg) Close observation
anaemia
coaguiopathy (fresh frozen plasma 10 ml/kg
and vitamin K) Repeated review
Central venous access required,
CXR, and urinary catheter
Consider adrenaline infusion
if poor response to volume replacement
and dopamine/dobutamina infusion Transfer to intensive care
264
20. ORGANOPHOSPHATE (OP) POISONING
OP compounds and carbamates are two main classes of insecticides.
Commonly used organophosphates: methyl parathion (metacid) and dichlorovos (nuvan)
PATHOPHYSIOLOGY
Inhibition of the cholinesterase (AchE) by irreversibly binding to it; accumulation of acetylcholine
at the neural synapses; initial over stimulation eventual exhaustion and disruption of neural
transmission.
If left untreated OP forms a permanent bond with this enzyme inactivating it. This process, called
'aging' occurs 2-3 days after exposure; wks to months are required for the body to regenerate
inactivated enzymes. In contrast carbamates form a temporary bond to the enzyme allowing
regeneration over several hours.
Symptoms caused by carbamate toxicity are usually less severe than those seen with OP. Muscarinic,
nicotinic and CNS receptor stimulation.
ACUTE TOXICITY
The muscarinic (cholinergic) signs (caused by Organophosphates and Carbamates) can be
remembered by use of one of two mnemonics
SLUDGE/BBB
Salivation, Lacrimation, Urination, Defecation, Garlic odor, Emesis (with Pin-point
pupils), Bronchorrhea, Bronchospasm, Bradycardia
DUMBELS
Defecation, Urination, Miosis, Bronchorrhea/Bronchospasm/Bradycardia, Emesis,
Lacrimation, Salivation
The nicotinic effects: fasciculations
CNS effects (probably through muscarinic and nicotinic receptors in the brain):
Respiratory depression, lethargy, excitability, seizures, coma
(2) INTERMEDIATE SYNDROME (IMS)
IMS occurs 24-96 hours after exposure. It arises between the early cholinergic syndrome and
late onset peripheral neuropathy. Bulbar, respiratory and proximal muscle weakness is
prominent. This resolves in 1-3 weeks.
(3) DELAYED PERIPHERAL NEUROPATHY
265
Occurs several weeks after exposure. Primarily motor involvement. May resolve
spontaneously or result in permanent neurological dysfunction
266
TREATMENT OF ACUTE TOXICITY
Therapy depends on severity; mildest cases need only observation, aggressive
cardiorespiratory support for seriously intoxicated.
Identify the type of ingestion, time interval, current symptoms, amount ingested.
Average swallow 5-10 ml (young child) 10-15 (older child)
Protect yourselves with gloves
ABC
Give 100% oxygen, early intubation may be required
Skin decontamination; wash with soap and water twice, remove contaminated clothes.
Gastric lavage: If ingestion within one hour of presentation

• Single dose of activated charcoal 1g/kg (maximum dose 50 gm) is given for gastric lavage. If the
patient is vomiting persistently, lavage is not necessary. Ensure that airway is protected.
• Forced emesis is contraindicated because of the risk of aspiration and seizures
Atropine: Specific antidote for muscarinic effects
• >12 yrs initial dose 1-2 mg; <12 yrs 0.05 mg/kg IV
• Repeat the dose every 3-5 minutes until atropinization occurs which is indicated by clearing of
bronchial secretions and ceasation of wheezing. Do not rely on pupillary changes;
• Maintain atropinization by giving every hour 20-30% of the total amount that was required to
atropinize. Maintain full atropinization for 2-3 days. Then atropine dose is daily reduced by 1/3
to ¼ of the dose given on the previous day.
• Continuous intravenous infusion of atropine may be necessary when atropine requirements are
massive and the dose is 0.02 to 0.08 mg/kg/hr, depending on the degree and stage of intoxication.
Hundreds of milligrams may be needed over several days in severe poisonings
• Signs of improvement after 12-24hrs are indications to begin gradual tapering of atropine doses.
• TACHYCARDIA AND MYDRIASIS ARE NOT CONTRAINDICATIONS TO ATROPINE

USE
• Inhaled ipratropium 0.5 mg with parenteral atropine may be helpful for bronchospasm; may repeat
• Atropine blocks the acetylesholine receptor and so is effective in both OP and carbamate
poisoning.
Pralidoxime: Bound AchE is reactivated by this drug; relieves nicotinic as well as muscarinic
267
effects; should be administered as early as possible in severe poisoning
• >12 yrs 1 - 2 g IV infusion over 30 min; <12 yrs 25 mg/kg over 30 min
• May repeat after 30 minutes or give continuous infusion if severe
• Continuous infusion at 10 mg/kg/hour in children
• If no IV access, give pralidoxime 15 mg/kg IM in children <40 kg (>40 kg- 600mg). Rapidly
repeat as needed to total of 1800 mg or 45 mg/kg in children.
• Pralidoxime should NOT be administered without concurrent atropine in order to prevent

worsening symptoms due to transient oxime-induced acetylcholinesterase inhibition
It chemically breaks the bond between the OP and the enzyme liberating the enzyme and degrading
the OP. Only effective before the bond 'ages' and becomes permanent. Not necessary for carbamate
because bond between insecticide and enzyme degrades spontaneously.
Benzodiazepine:
• Diazepam 0.1 to 0.2 mg/kg, repeat as necessary if seizures occur. Do not give phenytoin.
Patient should be observed for 24 hrs after the last dose of atropine.
268
21. EYE INFECTIONS
If an ocular infection occurs soon after birth and following a vaginal delivery, it was probably acquired
perinatally. The most important infections to consider are chlamydia, gonococcus and herpes simplex
virus (HSV).
A swab for culture and gram staining should be taken. Obtain results of gram stain before starting
treatment. If results are positive, consider treating mother and her partner. Bacterial conjunctivitis
should respond to frequent topical antibiotics. Use Gentamicin eye drops unless there is a specific
contraindication. Specific infections should have specific treatment as follows:
1. Gonococcal infections. These are very serious and can cause perforation of the eye.
Treatment is cefotaxime 100mg/kg single dose IM.
2. Chlamydia can give a sticky eye and may not present until the second postnatal week. Suspect if
persistent symptoms and no growth on routine swab. Although it is
normally a lower grade infection than gonococcus, it may be difficult to distinguish
them except by swab and scrape results. Treatment is normally topical tetracycline
ointment for 3 weeks as well as systemic erythromycin for 2 weeks.
3. HSV will require treatment with acyclovir ointment five times a day to the eye and
systemic treatment with acyclovir ointment five times a day to the eye and systemic
treatment may need to be considered.
Intra-uterine infection with toxoplasmosis, syphilis, rubella, can produce corneal opacities, cataract
and chorio-retinal scarring. There is no treatment which will restore retinal tissue structure. Flare
ups of posterior uveitis from congenital toxoplasmosis can occur in later life causing reduced
vision. Parents should be told about such disease as future flare ups, if sight threatening, will need
systemic treatment.
269
22. OTHERS
I. RULES OF THUMB FOR EXPECTED INCREASE IN WEIGHT
Age Expected Weight Increase
Birth -3 months 30g/day

Regain birth weight by 2 weeks
3-6 months 20 g/day

Double birth weight by 4-6 months
6-12 months 10g/day

Triple birth weight by 12 month
1-2 years 250g/month

2 years- adolescence 2.3 kg/year
30 g = 1 ounce body weight
II. RULES OF THUMB FOR EXPECTED INCREASE IN HEIGHT

Age Expected Height Increase
0-12 months 25 cm/year
Birth length increases by 50% at 12 months
13-24 months 12.5 cm/year
2 years-adolescence 6.25 cm/year

Birth length doubles by age 4 years
Birth length triples by age 13 years
270
III. RULES OF THUMB FOR EXPECTED INCREASE IN HEAD CIRCUMFERENCE
Age Expected Height Circumference Increase
Preterm upto 40 wks gest. 0.75 to 1.25 cm/week
0-2 months 0.5 cm/week
2-6 months 0.25 cm/week
By 12 months Total increase = 12 cm since birth
IV. PAEDIATRIC NORMAL VALUES FOR VITAL SIGHS

Age Resp rate Heart rate Systolic BP Blood vol
(years) (breaths/mi (beats/min (mm Hg) (ml/kg)
<1 30-40 110-160 70-90 85-90
2-5 20-30 95-140 80-100 75-80
5-12 15-20 80-120 90-110 65-70
>12 12-16 60-100 100-120 65-70
V. NORMAL HEMOGLOBIN LEVELS

Hemoglobin Hematocrit
(G/dl) (%)
Age Mean -2 SD Mean -2 SD
Birth (Cord Blood) 16.5 13.5 51 42
1 to 3 days (Capiliary) 18.5 14.5 56 45
1 week 17.5 13.5 54 42
2 weeks 16.5 12.5 51 39
1 months 11.5 9.0 43 31
2 months 11.5 9.0 35 28
3 to 6 months 11.5 9.5 35 29
0.5 to 2 years 12.0 10.5 36 33
2 to 6 years 12.5 11.5 36 33
6 to 12 years 13.5 11.5 40 35
12 t 18 years
Female 14.0 12.0 41 36
Male 14.5 13.0 43 37
18 to 49 years
Female 14.0 12.0 41 36
Male 15.5 13.5 47 41
• These data have been compiled from several sources. Emphasis is populations that are
likely to exclude individuals with iron deficiency normal population
271
VI. NORMAL BLOOD PRESSURE IN CHILDREN
Age Systolic Diastolic

Birth (12hrs, <1000gm) 39-59 16-36
Birth (12hrs, 3kg) 50-70 25-45
Neonate (96hrs) 60-90 20-60
Infant (6mths) 87-105 53-66
Toddler (2yrs) 95-105 53-66
School age (7yrs) 97-112 57-71
Adolescent (15yrs) 112-128 66-80
VII. NORMAL HEART RATE IN CHILDREN
Age Awake rate Mean Sleeping Rate

Newborn - 3mths 85-205 140 80-160
3mths - 2yr 100-190 130 75-160
2yrs – 10 yrs 60-140 80 60-90
>10yrs 60-100 75 50-90
VIII. NORMAL RESPIRATORY RATE IN CHILDREN
Age RR
Newborn 40
lyr 30
5yrs 20
10yrs 18
>10yrs 18
IX. APPROXIMATE AVERAGE HEIGHT AND WEIGHT FOR NORMAL CHILDREN

Age Kg
3 - 12mths Age (months) + 9
2
1 - 6yrs Age (yrs) x 2 +8
7 - 12yrs Age (yrs) x 7 - 5

2
Age Length/ Height (cm)

At birth 50cm
lyr 75cm
2-12yrs Age(yrs) x 6+77
272
X. INTRAVENOUS FLUID REQUIREMENTS
Body weight Fluid requirement per Fluid requirement per
First 10 kg 100 ml/kg 4 ml/kg
Second 10 kg 50 ml/kg 2 ml/kg
Subsequent kg 20 ml/kg 1 rnl/kg
The standard fluid bolus in shock is 20 ml/kg. for children, and 10ml/kg for neonates
Fever increases requirements by 12% for each degree Celsius rise.
XI. DAILY ELECTROLYTE REQUIREMENTS

Sodium 2-3 mmol/kg/day
Potassium 2-3 mmol/kg/day
XII. PLEURAL EFFUSIONS

Transudate Purulent Empyema Complicated
WBC 1000 5300 25900 55000

PMN% 50% >90% >95% >95%
Pr(fluid):Pr (Serum) <0.5 >0.5 >0.5 >0.5
LDH <200 >200
Glu >60 <60 <60 <40
PH 7.4-7.5 7.35-7.45 7.2-7.35 <7.2
Investigations to be sent
Serum: Protein and Glucose, CBC, ESR (+\- Blood culture, mantoux test)
Plural fluid: Protein, Glucose, pH, microscopy (Gram staining and AFB), culture
Indications for chest tube: PH 7.0 - 7.2, Glucose <40, gram stain shows organisms, purulent
fluid
XIII. ASCITIC FLUID

Transudate Exudate
SpGr <1.016 >1.016
<3G% >3G%
A fluid (Gradient) >1.1 <1.1
Fluid : serum Glucose >i <1
LDH <200IU >200IU
WBC <250-500 >1000 Usually with inf. PMN >250
(Nelson says >250 cells with >50%
PMN)
PH with Peritonits<7.35
273
Investigations to be sent
Serum: Albumin and Glucose
Ascitic fluid: Albumin, Glucose, pH, microscopy (Gram staining and AFB, culture)
If exudative, consider TB. If transudative, possible differential diagnoses include CHF, liver
disease, hypoalbunimaemia.
XIV. PERICARDIAL EFFUSIONS
Transudate Exudates
Cells Low High

Pr gm/dc < 3g/dc >3
Fluidr:Serum Pr <0.5 >0.5
Fluid:Serum glucose >1 <1
Specific gravity <1.015 >1.015
Fluid:Serum LDH <0.6 >0.6
Investigations to be sent:
Blood for CBC, glucose,(+_BC if probable Dx of staph),ESR
Mantoux, CXR, Echo

Pericardial fluid - Protein / Glucose, microbiology (Gm stain), culture
If acute History, with high fever and exudative fluid start clox and gent. If History is suggestive
of TB, the fluid is a transudate, and the patient is comfortable wait for TB investigations, if the
child is in distress start Category 1 ATT plus steroids.
References:
1. Nelson Text Book of Pediatrics, 19th edition.
2. O. P Ghai, 8th edition.
3. Principles of Pediatric & Neonatal Emergencies, 2nd edition.
4. Up To Date 18.2
274
XV. BLOOD CULTURE COLLECTION
Aim - collection of appropriate blood volume to allow growth of significant bacteria, using a sterile
technique to avoid contamination by skin flora.
Blood culture draw should be done PRIOR to antibiotic administration
1) Apply tourniquet, palpate and identify peripheral vein for blood draw.
2) Wearing gloves (non-sterile) clean overlying skin with 2% Iodine and wait 30
seconds. Alternatively, use Betadine but you must wait 1 minute, 10% iodine-
povidine 2 min; 0.5% chlorhexidine lmin. Cleaning the skin well pre-culture draw is
the most important factor in reducing contamination rates.
3) Remove plastic cap from Bactec bottle and clean rubber cap with 2%iodine/betadine
(leave to dry as for skin).
4) Without re-palpating vein, draw l-3ml blood with needle/butterfly and syringe or if
inserting a NEW cannula, it is acceptable to withdraw the first blood flush through
the hub using a clean needle attached to a syringe. DO NOT TAKE BLOOD
CULTURE SAMPLES FROM EXISTING CANNULAS/LINES.
5) NOTE: for each extra lml of blood (up to 3ml) there is an extra 10% yield
6) Inject blood into Bactec bottle. There is no need to change needles. (Evidence
suggests contamination rates are un-altered and risk of needlestick injury is higher
with needle change.)
7) Ensure bottle fully labeled and send to lab as quickly as possible. Bacteria may die if not stored
at appropriate temperature.
275
XVI. ASSESSMENT OF DEVELOPMENTAL MILESTONES
276
277
278
279
XVII. GUIDELINES FOR PHOTOTHERAPY IN NEONATAL JAUNDICE
(Modified from NICE guidelines, 2010)
Gestational age 12 HOL 24 HOL 36 HOL 48 HOL 60 HOL ≥72 HOL
27 weeks 3.3 4.4 5.5 7.2 8.3 9.4
28 weeks 3.3 5.0 6.1 7.2 8.8 10.0
29 weeks 3.3 5.0 6.3 7.7 9.1 10.5
30 weeks 3.8 5.0 6.6 8.3 9.4 11.1
31 weeks 3.8 5.5 6.9 8.3 10.0 11.6
32 weeks 3.8 5.5 7.2 8.8 10.5 12.2
33 weeks 3.8 5.5 7.5 9.1 11.1 12.7
34 weeks 4.0 6.1 7.7 9.4 11.6 13.3
35 weeks 4.0 6.1 7.7 10 11.9 13.8
Total serum bilirubin values have been converted to mg/dl
280
Manual of Neonatal Care (Cloherty). Seventh Edition
XVIII. GUIDELINES FOR EXCHANGE4 TRANSFUSION IN NEONATAL JAUNDICE

(Modified from NICE guidelines, 2010)
Gestational age 12 HOL 24 HOL 36 HOL 48 HOL 60 HOL ≥72 HOL
27 weeks 6.1 8.3 9.7 11.1 13.3 15.0
28 weeks 6.1 8.3 10.0 11.6 13.8 15.5
29 weeks 6.1 8.3 10.2 12.2 13.8 16.1
30 weeks 6.1 8.3 10.2 12.7 14.4 16.6
31 weeks 6.6 8.3 10.2 12.7 15.0 17.2
32 weeks 6.6 8.8 11.1 13.3 15.5 17.7
33 weeks 6.6 9.1 11.3 13.6 16.1 18.3
34 weeks 6.6 9.4 11.6 13.8 16.6 18.8
281
35 weeks 6.6 9.4 11.6 14.4 16.9 19.4
Total serum bilirubin values have been converted to mg/dl
Manual of Neonatal Care (Cloherty). Seventh Edition
XIX. NORMAL VALUES FOR THYROID FUCTION TESTS IN CHILDREN
XX. INDICATIONS FOR PICU ADMISSSION

Respiratory
282
1. Endotracheal intubation or potential need for endotracheal intubation and mechanical
ventilation
2. Rapidly progressive pulmonary disease with risk of progression to respiratory failure and/or
total obstruction
3. High supplemental oxygen requirement needing continuous moitoring
4. Newly placed tracheostomy with or without the need for mechanical ventilation
5. Requirement for more frequent or continuous inhaled or nebulized medications than can be
administered safely in pediatric ward (as in severe asthma, croup etc)
6. Pneumothorax requiring chest tube insertion
Cardiovasular
1. Shock not responding to fluid resuscitation
2. Postcardiopulmonary resuscitation;
3. Life-threatening dysrhythmias
4. Unstable congestive heart failure
5. Congenital heart disease with unstable cardiorespiratory status
6. Patients requiring pericardiocentesis
Neurological
1. Seizures (including status epilepticus), unresponsive to therapy or requiring continuous

infusion of anticonvulsive agents
2. Coma with the potential for airway compromise
3. Progressive neuromuscular dysfunction requiring cardiovascular monitoring and/or

respiratory support (e. g. ascending paralysis in GBS)
4. Patients with an acutely diminished level of consciousness or a decreasing level of

consciousness
5. Raised ICP
Renal
1. Acute renal failure with significant fluid/electrolyte imbalance
Postoperative
283
1. Patients who have undergone major surgery
2. Patients requiring intensive cardiorespiratory care and monitoring
3. Severe coagulopathy
4. Severe anemia resulting in hemodynamic and/or respiratory compromise
Endocrine/Metabolic
1. Severe diabetic ketoacidosis
2. Other severe electrolyte abnormalities, such as:
a. Hyperkalemia, requiring cardiac monitoring and acute therapeutic intervention
b. Severe hypo- or hypernatremia
c. Hypo- or hypercalcemia
d. Hypo- or hyperglycemia requiring intensive monitoring
e. Severe metabolic acidosis requiring bicarbonate infusion or intensive monitoring
f.Need for central venous or arterial catheter insertion
Gastrointestinal
1. Severe acute gastrointestinal bleeding leading to hemodynamic or respiratory instability
2. Acute hepatic failure leading to coma, hemodynamic, or respiratory instability
Others
1. Toxic ingestions and drug overdose with potential acute decompensation of major organ
systems
2. Multiple organ dysfunction syndrome
3. Electrical or other household or environmental (eg, lightning) injuries
284
Information for Residents
Training that are being run by department
S.no Training Description Frequency

1. Primary Trauma Care Two days trauma training Once a year
certified by PTC foundation
2 Palliative care Two days training focusing on Once a year
management of terminally ill
patient. Certified by Palliative
care, Nepal
3. Basic Assessment and Support Basic critical care training run Once a year
of Seriously il patients in by PAHS in collaboration with
developing health care systems Basic DHS team
(Basic DHS)
4 ACLS In house training As per needed
5 Nepal BLS In house training As per needed
6 Simulations Hands on short sessions Once a week

PAHS - Emergency Department Protocol

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PAHS - Emergency Department Protocol

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Emergency

Patan Academy of Health Sciences

Communicaiton skills 1-4

Clinical examinations 5-25

Emergency structure and operation 26-32

Cardiac emergencies 68-79

Respiratory emergencies 80-97

Abdominal emergencies 98-119

Neurological emergencies 120-131

Metaboic emergencies 132-147

Common problems 168-180

Environmental injuries 181-184

Orthopedic injuries 185-192

Obstetrics and Gynecology emergencies 193-197

Psychiatry emergencies 198-199

Police cases 200-202

Paediatric emergencies 222-284

Crisis Resource management (CRM)

Three big CRM skills are

Close loop communication

Sharing information (SBAR)

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 2

Delivering death notification

What reaction to expect?

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 3

Besides these principles, we can use some other theories like

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 4

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 5

o Migratory thrombophlebitis in Ca panceas

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 6

Fever with exanthema

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 7

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 8

• Crowding of ribs, Kyphosis or Scoliosis

Irregular Abnormal Breathing Pattern

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 9

Inspiratory Tracheal descent

Tenderness over chest wall

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 10

posteriorly by trapezius. Percussion is done by standing behind patient. Hyper resonance –

Lateral chest wall

Posterior chest wall

Percussion on right side

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 11

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 12

Jugular Venous Pressure

Causes of elevated JVP

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 13

Unilateral non pulsatile Innominate vein thrombosis

Chest wall defects: Pectus excavatum, Pectus carinatum

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 14

Abnormalities of apical impulse

Shocks: Palpable heart sound

Thrills: Palpable murmur – base of fingers

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 15

S4: Hypertrophic cardiomyopathy, HTM, CAD

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 16

Uncommon mid diastolic murmurs

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 17

Visible gastric peristalsis (VGP) or intestinal peristalsis (VIP)

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 18

o SVC obstruction: Blood flow in vein is caudally above umbilicus.

DEPARTMENT OF GENERAL PRACTICE AND EMERGENCY MEDICINE 19