Department of Emergency Medicine

Operating Manual

Section II – Medical Care Pathway

Contents
Section II - Medical Care Pathway ................................................................... 4
Basic Life Support Algorithm ............................................................................................................... 4
Management of Adult Tachycardia with pulse ................................................................................... 7
Management of Adult Bradycardia with a Pulse – ............................................................................. 8
Management of Acute Coronary Syndrome – .................................................................................... 9
Approach To The Diagnosis Of Chest Pain ........................................................................................ 10
Algorithm for Diagnosis and Management of Chest Pain ................................................................. 11
Stroke Management ......................................................................................................................... 15
NIHSS Scale –................................................................................................................................. 18
Sepsis and Septic Shock .................................................................................................................... 19
Algorithm for Suspected Sepsis Patient in the Emergency – ............................................................ 21
Diabetic Ketoacidosis ........................................................................................................................ 23
Flowchart for DKA management................................................................................................... 24
Flowchart for DKA management................................................................................................... 25
Hypoglycemia .................................................................................................................................... 26
Anaphylaxis ....................................................................................................................................... 28
Emergency Treatment of Severe Asthma ......................................................................................... 31
Management of COPD ...................................................................................................................... 35
NIV Guidelines................................................................................................................................... 38
Management of Pneumonia ............................................................................................................. 42
Moderate- and high-severity community-acquired pneumonia .................................................... 43
Acute Kidney Injury ........................................................................................................................... 44
1) Hyperkalaemia ...................................................................................................................... 47
2) Pulmonary oedema................................................................................................................ 49
3) Acidosis................................................................................................................................. 49
4) Fluid balance ......................................................................................................................... 50
5) Dopamine .............................................................................................................................. 50
6) Diuretics ................................................................................................................................ 50
7) Relief of obstruction ............................................................................................................. 50
8) General measures .................................................................................................................. 51
The Altered Sensorium Patient – Unconsciousness, Syncope, Confusion ........................................ 52
Seizures in an Adult........................................................................................................................... 54
Status Epilepticus .............................................................................................................................. 56
Intracranial Pressure ......................................................................................................................... 58
Poisoning – General Approach and Specific Drug Ingestions ........................................................... 61
Acetaminophen Poisoning ................................................................................................................ 68
Pesticide Poisoning ........................................................................................................................... 73
Organophosphorus Poisoning ....................................................................................................... 73
Rodenticide Poisoning – Rat Poison ingestion .............................................................................. 79
Corrosive Ingestion ........................................................................................................................... 82
Snake Bite.......................................................................................................................................... 85
ASV reaction - Approximately 20% patients treated with ASV develop reactions. ..................... 92
Treatment of ASV reaction ........................................................................................................... 92
Scorpion Sting ................................................................................................................................... 96
Dog Bites and Other bites ................................................................................................................. 97
Treatment Algorithm for Rabies ..................................................................................................... 101
Burns ............................................................................................................................................... 102
Thermal Burns ............................................................................................................................. 102
Chemical Burns –......................................................................................................................... 105
Electrical Burns and Injuries ........................................................................................................ 106
Dengue ............................................................................................................................................ 108
Treatment of Moderate Dengue – DHF I and II .......................................................................... 110
Treatment of Severe Dengue – DHF III ....................................................................................... 111
Treatment of Severe Dengue – DHF IV ....................................................................................... 112
Gastrointestinal Bleed..................................................................................................................... 114
ABG Interpretation.......................................................................................................................... 116
Procedure for Radial ABG - ......................................................................................................... 116
Interpretation.............................................................................................................................. 118
 Section II - Medical Care Pathway

Basic Life Support Algorithm(1)

Note: According to the 2015 ACLS update

aThe chest compression rate is 100-120/ min
b Give 1 breath every 6 seconds (for respiratory arrest
Management of Cardiac Arrest –
Management of Adult Tachycardia with pulse
Management of Adult Bradycardia with a Pulse –
Management of Acute Coronary Syndrome –
Approach To The Diagnosis Of Chest Pain(2–4)

For acute chest pain presenting to the Emergency Department with ECGs not showing
features of ST Elevation ACS, the HEART approach should be used to evaluate patients.

Parameter

History Highly suspicious 2

Moderate suspicion 1

Low suspicion 0

ECG Significant ST 2
Depression

Non Specific 1
repolarization
changes

Normal 0

Age <45yrs 2

45-64yrs 1

>65 yrs 0

Risk factors >3 risk factors or 2

h/o atherosclerotic
disease

1-2 risk factors 1

The approach is just a guideline since the specific diagnosis of chest pain requires integration
of data about the patient‘s risk factors, description of pain, and associatedNo risk factors
symptoms, as well 0
as the physical examination and electrocardiogram or chestTroponin
radiograph. > 3 times normal 2
Diagnostic algorithm — the initial step prior to following the algorithm below is to perform a
1-3 times normal 1
focused history and physical examination, and consider performing an ECG and/or chest x-
< Normal 0
ray. Derive at the specific cause of symptoms and begin treatment, after ruling out a cardiac
event the specific cause of symptoms and begin treatment.Low risk – 0-3 Risk of ACS – 0.9-1.7%
Moderate risk – 4-6 Risk of ACS – 12 – 16.6%
High Risk 7-10 Risk of ACS – 50-70%
Algorithm for Diagnosis and Management of Chest Pain
Step 1 (Evaluate need for emergent care) — Consider potentially life-threatening causes of
chest pain. Patients in whom an acute coronary syndrome (acute myocardial infarction or
unstable angina) is suspected should receive emergent care (this generally includes chewing
an aspirin, nitroglycerine, morphine, oxygen)
Emergency care should also be provided to patients who appear to be seriously ill and to
patients in whom there is a suspicion of a critical non-coronary diagnosis such as pulmonary
embolus, pneumothorax, aortic dissection, oesophageal rupture, or acute abdomen. For
patients who do not require emergent care, proceed to Step 2.
Step 2 (Emergent care not needed) — In patients in whom a diagnosis of stable CHD appears
likely based on symptoms that are suggestive of angina and/or a history of cardiac risk
factors, proceed to Step 3; otherwise, proceed to Step 5.
Step 3 (Symptoms consistent with stable angina) — Evaluate the patient for CHD, and
consider starting outpatient management (therapy may include aspirin, beta blockers,
nitroglycerin, and education about the need for emergency care) or admitting the patient to
the hospital, especially if symptoms are progressive. If there is a concern for angina
secondary to valvular heart disease (eg, critical aortic stenosis), perform an echocardiogram
prior to stress testing. Consider other causes of chest pain, such as cardiac syndrome X and
pulmonary hypertension. If the results of the evaluation do not demonstrate CHD, proceed to
Step 4; otherwise, proceed to step 8.

Step 4 (Evaluation for CHD was negative) — Evaluate the patient for gastrointestinal
disease. This evaluation may initially involve a trial of acid suppression. If there is no
diagnosis and symptoms persist, proceed to step 6; otherwise, proceed to step 8.
Step 5 (Symptoms not suggestive of angina)
Step 5a— For patients who are felt not to have an ischemic etiology for chest pain but who
have significant risk factors for CHD, consider arranging for an evaluation for CHD –stress
testing
Step 5b— If symptoms suggest a musculoskeletal etiology, a trial of an NSAID is
appropriate; otherwise, proceed to step 5c. If pain persists, consider rib films, a bone scan,
and plain or CT chest radiography.
If there is no diagnosis and symptoms persist, proceed to step 6; otherwise, proceed to step 8.
Step 5c— If symptoms suggest a gastrointestinal etiology, evaluate the patient for
gastrointestinal disease; otherwise, proceed to step 5d. This evaluation may initially involve a
trial of acid suppression.
If there is no diagnosis and symptoms persist, proceed to step 6; otherwise, proceed to step 8.
Step 5d— If symptoms suggest a psychogenic etiology, evaluate the patient for a
psychosocial source of chest pain otherwise, proceed to step 5e. Diagnostic strategies may
include a therapeutic trial of an antidepressant medication or a psychiatric referral. If there is
no diagnosis and symptoms persist, proceed to step 6; otherwise, proceed to step 8.
Step 5e— Consider chest anatomy as a guide to other less common causes of non-life-
threatening chest pain including: chest wall pain (eg, zoster, breast disease); other cardiac
pain such as pericarditis; pathology of the lung parenchyma, vasculature, or pleura; and pain
referred to the chest from the gallbladder, diaphragm, or from a disc herniation.
Step 6 (Persistent chest pain) — If chest pain persists and evaluations for CHD (as in step
5a), musculoskeletal pain (as in step 5b), gastrointestinal pain (as in step 5c), psychogenic
pain (as in step 5d), and other causes (as in step 5e) have not all been performed, those
evaluations should now be undertaken. If there is no diagnosis and symptoms persist, proceed
to step 7; otherwise, proceed to step 8.
Step 7 (Diagnostic evaluations negative) — Patient likely has chronic idiopathic chest pain.
Since this is known to cause significant disability, consider referral to a pain management
center or medical symptom reduction program. No further evaluation is required unless the
patient has a change in symptoms or the symptoms are disabling.
Step 8 (Cause of chest pain diagnosed) — Proceed with therapy or additional evaluation as
appropriate for the diagnosed condition.
Additional information to expand the algorithm –
 The clinician‘s first step in the evaluation of any patient with recent chest discomfort
is to exclude life-threatening illness, including ACS, pulmonary embolism, aortic
dissection, pneumothorax and oesophageal rupture. ACS is the most common of the
aetiologies requiring immediate hospitalization.
 Consideration of all information in the history, physical examination, ECG, and chest
radiograph will determine whether ACS or alternative diagnoses are more or less
likely. In patients for whom the likelihood of ACS is neither high nor low, decisions
will need to be made in part based upon patient proximity to a health care facility,
ability to comply with specific provider recommendations, family support system and
patient and practitioner preferences.
 Patient features, any one of which should alert the clinician to a high likelihood of
ACS in a patient who does not have clear ST elevations on ECG, include
o Worsening in the frequency, intensity, duration, and timing (eg, nocturnal
pain, rest pain) of prior history or equivalent symptoms
o New onset symptoms of shortness of breath, nausea, sweating, extreme fatigue
in a patient with a known history of cardiovascular disease
o Onset of typical symptoms in a patient without a history of CVS disease
o New findings on physical examination of murmur, hypotension, diaphoresis,
rales or pulmonary edema
 o Transient ST deviation (≥ 1 mm) or T wave inversion in multiple precordial
leads.
 Features that need to be considered but are not as predictive as the high likelihood
ones include
o Age greater than 70 years
o Diabetes mellitus
o Extracardiac vascular disease
o Either fixed Q waves or ST depression of 0.5 to 1 mm or T-wave inversion >
1mm on ECG.
 Emergent hospitalization is necessary for patients with suspected acute myocardial
infarction or, usually, unstable angina
o Exercise stress testing is indicated for patients with a suspected ischemic heart
disease who do not have an unstable coronary syndrome (eg, acute myocardial
infarction or unstable angina). The indications and options for exercise testing
are discussed in detail separately.)
o Transthoracic echocardiography (TTE) can identify regional wall motion
abnormalities within seconds of acute coronary artery occlusion and is a useful
adjunct to the standard evaluation for cardiac ischemia. TTE is also
appropriate to assist in the identification of other causes of chest pain, such as
pericarditis with effusion, aortic dissection, and possibly pulmonary
embolism.
o Cardiology consultation should be considered when the diagnosis is not clear.
o Empiric treatment with aspirin, beta blockers, and/or sublingual nitroglycerin
is indicated in a patient who has a high likelihood of ischemic coronary
disease on the basis of the clinical evaluation while awaiting a diagnostic test
o A diagnosis of chest wall pain should not be made until other causes have
been thoughtfully excluded:
o Patients with active myocardial ischemia can also have chest wall tenderness
that may or may not be reproducible by palpation
o Other causes of ―pleuritic‖ chest pain, such as pulmonary embolism, must also
be considered. A reduced PaO2 or increased alveolar-arterial gradient may
suggest the diagnosis of pulmonary embolism; however, the PaO2 is between
85 and 105 mmHg in approximately 18 percent of patients with pulmonary
embolism, and up to 6 percent may have a normal alveolar-arterial gradient for
oxygen Of note, chest pain due to pulmonary embolism may be persistent
rather than pleuritic.
Stroke Management(1,5)
 Step 1 – Patients presenting with suggestive of stroke to the Emergency Department will
immediately be shifted to the Red Zone (Resus Zone) from triage.
 Step 2 – Airway, Breathing and Circulation will be assessed and stabilised following
which Face-Arm-Speech test will be done initially. GRBS must be checked for all such
patients.
 Step 3 – Iv line will be started and Samples collected and patient will be connected to the
monitor.
 Step 4 – ECG must be done for all patients with suspected stroke.
 Step 5 – Time of onset of symptoms and brief history will be taken. Patient‘s NIHHS
score will be calculated and CT will be planned for the patient.
 Step 6 – CT shall be done and reported with a target time of 45 minutes from ED arrival.
 Step 7 – If CT shows no bleed, patient will be given Aspirin 150mg and Atorvastatin
40mg and fibrinolytic checklist shall be used to check if patient is a candidate for
fibrinolysis. If so, then consent shall be taken from the patient and thrombolysis shall be
performed with rTPA followed by admission in the ICU under Medicine. Neurologist
shall be consulted in case of doubtful diagnosis.
 Step 8 – If CT shows Intracranial bleed or ICSOL with Oedema causing symptoms,
Neurosurgery consult shall be taken. Anti-oedema measures should also be considered.
NIHSS Scale –
Sepsis and Septic Shock(6,7)
The definition of Sepsis was updated in 2017 – ―A life-threatening organ dysfunction caused
by a dysregulated host response to infection.‖ End organ damage is identified as an acute
change in total Sequential [Sepsis-related] Organ Failure Assessment score (SOFA) ≥2.
(Rhodes 2017)
Septic shock: A subset of sepsis ―in which circulatory, cellular, and metabolic abnormalities
are associated with a greater risk of mortality than with sepsis alone. These patients can be
clinically identified by a vasopressor requirement to maintain a MAP ≥ 65mmHg and serum
lactate >2mmol/L in the absence of hypovolemia‖ (Singer 2016)
―Severe sepsis‖ category was deemed to be superfluous and is no longer recommended for
clinical use
SIRS criteria is no longer considered in defining sepsis and septic shock
Instead, adult patients outside of the ICU with suspected infection are identified as being at
heightened risk of mortality if they have quickSOFA (qSOFA) score meeting ≥2 of the
following criteria: respiratory rate of 22/min or greater, altered mentation, or systolic blood
pressure of 100mmHg or less (Singer 2016)

Patient with
suspected
infection

Calculate qSOFA
score > 2

<2 >2

SOFA > 2
Sepsis Still
suspected
Sepsis

Despite adequate fluid,

Monitor CLinical Vasopressor
status and required/Serum LActate
reevaluate > 2mmol/l
periodically

Septic Shock
HOUR ONE BUNDLE: INITIAL RESUSCITATION FOR SEPSIS AND SEPTIC
SHOCK (BEGIN IMMEDIATELY):
1. Measure lactate level with ABG
2. Obtain blood cultures before administering antibiotics.
3. Administer broad-spectrum antibiotics.
4. Begin rapid administration of 30ml/kg crystalloid for hypotension or lactate ≥4
mmol/L.
5. Apply vasopressors if hypotensive during or after fluid resuscitation to maintain a
mean arterial pressure ≥ 65 mm Hg. Initial choice of Vasopressor – Noradrenaline.
Monitor glucose levels every 1-2 hours and Target Glucose levels of < 180mg/dl.
Note – Consider hydrocortisone only BP cannot be maintained with aggressive fluid
resuscitation and vasopressors. (Hydrocortisone 200mg)
 Algorithm for Suspected Sepsis Patient in the Emergency –

0 Minutes
Patient with suspected
Sepsis

qSOFA score -
Altered Mental Status GCS
< 15
Respiratory Rate >22
SBP < 100mm Hg

Fluid
Monitoring Investigations Antibiotics Source Control
Resuscitation

30ml/kg IVF Continuous CBC, Creatinine, Start as soon as Identify source of

within first 3 monitoring of PR, S/E, BLood Culture, possible. DO NOT infection - Remove
hours RR, BP and spO2 BUN, Lactate, ABG, DELAY BECAUSE OF any indwelling
ECG, CXR Urinalysis CULTURE* catheters

Target initial MAP > 65mm Half hourly manual check Start Broad Spectrum
Hg Additional fluids based of vitals Antibiotic - Piperacillin
on reassessment Tazobactam/Cefperazone
-Sulbactam/Meropenem

60 Minutes *If Delay > 45 minutes – Administer Antibiotics stat.

Medicine department Senior on call will be informed about the patient.

Patient admitted in ICU/HDU depending on vitals and clinical condition for further care and
management.
Other supportive investigations and therapy –
 Intubation will be considered based on Airway patency, breathing effort, acidosis on the
ABG and sensorium of the patient. (Refer Ventilation guidelines)
 Reassessment in view of prolonged stay in ED –
o Re-measure Lactate if initial level is high.
o Dynamic Volume status reassessment –
 Repeated focused examn– vital signs, capillary refill and skin findings.
 Bedside cardiac ultrasound
 Passive leg raise test or fluid challenge.
 Do not use sodium bicarbonate therapy for the purpose of improving hemodynamics or
reducing vasopressor requirements in patients with hypoperfusion-induced lactic acidosis
with pH ≥7.15 (grade 2B).
 Ultrasound/CT will be considered if focus is suspected to be intra-abdominal. Imaging
will be performed from the emergency only if patient has maintained vital parameters for
a significant period and is not on vasopressors.
 Blood Product Administration
o Once tissue hypoperfusion has resolved and in the absence of extenuating
circumstances, such as myocardial ischemia, severe hypoxemia, acute
hemorrhage, or ischemic heart disease, we recommend that red blood cell
transfusion occur only when hemoglobin concentration decreases to <7.0 g/dLto
target a hemoglobin concentration of 7.0 –9.0 g/dL in adults (grade 1B).
o Fresh frozen plasma will not be used to correct laboratory clotting abnormalities
in the absence of bleeding or planned invasive procedures (grade 2D).
o In patients with severe sepsis, administer platelets prophylactically when counts
are <10,000/mm3 (10 x 109/L) in the absence of apparent bleeding. We suggest
prophylactic platelet transfusion when counts are < 20,000/mm3 (20 x 109/L) if
the patient has a significant risk of bleeding.
o Higher platelet counts (≥50,000/mm3 [50 x 109/L]) are advised for active
bleeding, surgery, or invasive procedures (grade 2D).
 Patients with severe sepsis should receive daily pharmacoprophylaxis against venous
thromboembolism (VTE) (grade 1B). This should be accomplished with daily
subcutaneous low-molecular weight heparin (LMWH) (grade 1B).
 Stress ulcer prophylaxis with Proton pump inhibitor or H2 Antagonist.
 Antiviral therapy initiated as early as possible in patients with severe sepsis or septic
shock of viral origin (grade2C).
 Targets ofresuscitation:
o Central venous pressure 8–12 mmHg
o Mean arterial pressure (MAP) ≥ 65 mmHg
o Urine output ≥ 0.5mL/kg/hr
o In patients with elevated lactate levels targeting resuscitation to normalize lactate.
Diabetic Ketoacidosis(7,8)

Diagnostic criteria: all three of the following must be present

 Capillary blood glucose above 11 mmol/L (>250mg/dl)
 Capillary ketones above 3 mmol/L or urine ketones ++ or more
 Venous pH less than 7.3 and/or bicarbonate less than 15 mmol/L
Typical deficits
 Water: 6 L, or 100 mL per kg body weight
 Sodium: 7 to 10 mEq per kg body weight
 Potassium: 3 to 5 mEq per kg body weight
 Phosphate: ~1.0 mmol per kg body weight
Factors Most Often Associated with the Development of Diabetic Ketoacidosis
Factor Approximate frequency (%)
Infection 35
Omission of insulin or inadequate insulin 30
Initial presentation of diabetes mellitus 20
Medical illness 10
Unknown 5

Key points in the management of DKA –

 GRBS must be checked for all patients above the age of 25 years and for all paediatric
cases. Specifically if the patient is complaining of episodes of vomiting GRBS must
be checked.
 All patients with GRBS >250mg/dl with dehydration, tachycardia, high ketones or
unstable vitals must be triaged to Red zone for further evaluation and assessment. The
presence of even mild signs of dehydration indicates that at least 3 L of fluid has
already been lost.
 ABG, ECG and Blood ketones will be performed for all patients with GRBS above
250mg/dl.
 Start two large bore iv cannulas and collect samples for CBC, Creatinine, Blood Urea,
Serum Electrolytes.
 Fluid resuscitation is the first key and most important step in the management of
DKA. Do not administer insulin before commencement of fluid resuscitation.
 Potassium correction must be started for patients with DKA based on the flowchart
below. If potassium is less than 3.5mmol/l insulin infusion must be delayed in order to
correct potassium first.
 Only short-acting insulin is used for correction of hyperglycemia in DKA.
 Subcutaneous absorption of insulin is reduced in DKA because of dehydration;
therefore, using intravenous routes is preferable.
 A small intravenous bolus can be considered if intravenous infusion is going to be
delayed or if resuscitation is ongoing. It offers no change in outcome.
 Target an infusion that reduces glucose by 100mg/dl/hour. Do not target a rapid
reduction of glucose as it can lead to hypoglycemia and increase in counter regulatory
hormones leading to rebound ketosis.
 Bicarbonate infusion does not affect outcomes in DKA with ph>6.9.
 When glucose falls below 200mg/dl, start the patient on 5% Dextrose infusion and
decrease the rate of insulin infusion by half.
 Reassess GRBS and vitals and blood ketones q1h. VBG q4h.
 Targets –
o Capillary ketones not falling by at least 0.5 mmol/L/hr
o Venous bicarbonate not rising by at least 3 mmol/L/hr
o Plasma glucose not falling by at least 3 mmol/L/hr
 If targets not met or response is inadequate increase infusion by 1u/hr

Flowchart for DKA management

Start Insulin infusion at

0.1U/kg/hour and continue
until ketosis and academia
resolve.
When Blood Glucose <
200mg/dl switch fluid to 5%
dextrose and half insulin
infusion rate
Flowchart for DKA management
Hypoglycemia(7)
Hypoglycemia is defined according to the following serum glucose levels:
a < 70 mg/dL in adults
b < 40 mg/dL in infants and children
If the cause of is other than oral agents or insulin in a diabetic patient, other lab tests may be
necessary.
The initial approach in the ED should include the following:
ABCs ( Airway, Breathing, C irculation)
Intravenous (IV) access
Oxygen
Monitoring
Glucometer
Administration of glucose as part of the initial evaluation of altered mental status often
corrects hypoglycemia. As was the case in the field, treatment should not be withheld while
one is waiting for a laboratory glucose value. Because the brain uses glucose as its primary
energy source, neuronal damage may occur if treatment of hypoglycemia is delayed.
A hypoglycemia patient with an altered mental status may receive a bolus of glucose. This
procedure is unlikely to harm the patient with high glucose; however, the delay in giving
glucose to the hypoglycemic patient may be detrimental.
If a glucometer reading can be performed immediately, it is reasonable to await the results
(which are typically available within 1 minute) before deciding whether to administer
glucose.
Once the diagnosis of hypoglycemia is made, search carefully for the cause in the previously
healthy patient. In the diabetic patient, potential causes of the hypoglycemia episode include
medication changes, dietary changes, new metabolic changes, recent illness, and occult
infection.
Management –
Regardless of the cause, management of hypoglycemia in the ED includesprompt diagnosis
and PO or IV administration of rapidly metabolizedcarbohydrates (i.e., glucose or dextrose).
In patients with altered mentalstatus, 50% dextrose in water is administered IV as a bolus
dose of 50 mL,which provides 25 grams of glucose. This dose may be repeated if
hypoglycaemia persists.
When the patient regains consciousness, carbohydratesshould be continued to prevent
recurrence of hypoglycemia. This can beaccomplished through PO administration of long-
acting carbohydrates orcontinuous IV infusion of dextrose (10% dextrose in water at a rate to
maintainthe serum glucose >100 milligrams/dL [5.55 mmol/L]).
Blood glucoseshould be determined every 30 minutes for the first 2 hours, looking
forrebound hypoglycemia. If hyperglycemia is maintained by slow administrationof dextrose,
the infusion may be reduced and eventually withdrawn.
Failure to respond to parenteral glucose administration shouldprompt consideration of
other causes, such as sepsis,toxin, insulinoma, hepatic failure, or adrenal insufficiency.
Hypoglycemiaresulting from sulfonylureas is much more challenging thaninsulin-induced
hypoglycemia. Hemodialysis and charcoal hemoperfusion,are not routinely recommended.
Admission criteria
Admission criteria for patients with acute hypoglycemia include the following:
 No obvious cause
 Oral hypoglycemic agent
 Long-acting insulin
 Persistent neurologic deficits
 Patients with no known cause or no previous episodes of hypoglycemia must be admitted.
Discharge criteria
 For patients on either short-acting insulin or hypoglycemic agents who have not eaten and
have had their hypoglycemia reversed rapidly, a high carbohydrate meal prior to
discharge is recommended.
Discharge may be considered after a high carbohydrate meal in the following situations:
 An obvious cause is found and treated
 The hypoglycemic episode is reversed rapidly
 A competent adult who has been directed to monitor fingerstick glucose measurements
closely during the remainder of the day should accompany the patient after discharge.
Discharging a patient following a episode that is likely the result of a long-acting oral
medication is a potential pitfall. Any patient for whom the cause is not identified readily may
have a recurrence of hypoglycemia with resultant sequelae.
Patients must be educated as to the causes and the early signs and symptoms of
hypoglycemia. This is particularly important for those patients who have a history of prior
episodes of hypoglycemia or who are newly diagnosed diabetics. General outpatient diabetic
education or inpatient diabetic teaching is indicated.
For overdose, accidental ingestion, or therapeutic misadventures with oral hypoglycemics,
little correlation exists between the amount of oral agent ingested and the length or depth of
coma. These patients require admission. Asymptomatic patients who have ingested
hypoglycaemic agents should be observed for the development of hypoglycemia, because the
onset of action and the half-life are extremely variable. The length of observation is based on
the ingested agent. Inadequate data are available to predict the extent or the time course of
hypoglycemia in children.
Anaphylaxis(9)
Definition – Severe, life-threatening generalized or systemic hypersensitivity reaction, which
is characterized by being rapid in onset with life-threatening airway, breathing or circulatory
problems, and is usually associated with skin, mucosal changes- eg, generalized hives,
pruritus or flushing, swollen lips-tongue-uvula (Not present in all patients).
Diagnose anaphylaxis if –
 Sudden onset symptoms with rapid progression
 Airway problems –
o Airway swelling and oedema
o Hoarseness
o Stridor
 Breathing problems –
o Dyspnoea and breathing difficulty
o Hypoxia
o Wheezing
o Cyanosis
o Respiratory arrest
 Circulation problems –
o Hypotension
o Signs of shock
o Decreased Sensorium
o Cardiac Arrest
Anaphylactic Reaction present?
2 or more of the following the occur after exposure to a
likely allergen for that patient:
(occurring within minutes to hours of exposure)
a. Involvement of the skin or mucosal tissue
b. Respiratory compromise
c. Reduced BP or associated symptoms
d. Persistent GI tract symptoms

Initiate second line therapy

Assess ABC - H1 & H2 antihistamines
Yes
Epinephrine (1:1000) IM - Glucocorticoid
Observation x 4-6 Hrs
Disposition decision

Good clinical response? If discharge:

72 Hrs Rx for
NO
- H1 & H2 antihistamines
Repeat IM Epinephrine Q5-15mins NO - Glucocorticoid
Airway/O2/IV/Cardiac monitor Follow up with PCP; if no PCP referral to
allergist
Albuterol if bronchospasm present
Administer second line therapy when available:
Caution while discharging in –
- H1 & H2 antihistamines Severe Reactions
- Glucocorticoid Possibility of continuity of allergen
Yes h/o Biphasic reaction
Poor social support
Hypotension/ Shock present?

Maintain Supine/ Trendelenberg position

IV fluids – 0.9% NaCl
Vasopressors
- Consider Epinephrine IV
- Dopamine
Glucagon if patient is on Beta blocker
Admit
Emergency Treatment of Severe Asthma(10–12)
Management of Severe Asthma – Emergency Department
Management of COPD(7,13,14)
Medical Assessment
History should focus on
 Current symptoms: cough, sputum colour and volume, breathlessness and chest pain.
 Usual exercise tolerance and exercise tolerance now.
 Smoking history: current, ex-smoker (>3 months) or never smoker.
 When started/stopped smoking, quantity per day and what (tobacco, cannabis, other)
 Pack years = number per day/20 x number of years smoking.
Previous treatment:
 Home oxygen – hours per day, flow rate, equipment
 Previously ventilated – invasive, non-invasive, domiciliary NIV (please note: specify
 CPAP or NIV as a home pressure support therapy)
 Evidence of chronic hypercapnic respiratory failure
Social history: abilities to perform activities of daily living, assistance required.
History and examination should look for signs of chest consolidation. Other causes of
breathlessness in someone with COPD should be sought, including cardiac ischaemia or
failure, pulmonary embolism, pneumothorax and uncontrolled AF. Signs of fluid overload
and hypovolaemia should be looked for and treated.
The diagnosis is suspected on the basis of symptoms and signs and supported by spirometry.
Suspect a diagnosis of COPD in –
 People over 35 who have a risk factor 8 (generally smoking or a history of smoking)
and who present with one or 9 more of the following symptoms:
o Exertional breathlessness
o Chronic cough
o Regular sputum production
o Frequent winter ‗bronchitis‘
o Wheeze
When thinking about a diagnosis of COPD, ask the person if they have:
 Weight loss
 Reduced exercise tolerance
 Waking at night with breathlessness
 Ankle swelling
 Fatigue
 Occupational hazards
 Chest pain Uncommon in COPD and raise the possibility
 Haemoptysis (coughing up blood) of alternative diagnoses
Investigations
All patients require FBC, RFTs, CXR and ECG.
All hypoxemic patients require ABG.
Sputum specimen should be sent for culture if cough is productive and blood cultures
should be sent if febrile.
Management
 Assess severity of symptoms
 Administer controlled oxygen to maintain target saturation of above 90%
 Continuous cardiovascular status monitoring
 Perform arterial blood gas measurement
 Administer bronchodilators
o β2-Agonists and/or anticholinergic agents by nebulization or metered-dose
inhalerwith spacer
o Sabutamolnebulisers 2.5mg qds
o Ipratropium bromide nebulisers 0.5mg qds
 Add oral or IV corticosteroids
o Prednisolone 30mg od for 7 days unless contraindication
 Consider antibiotics if increased sputum volume, change in sputum color, fever, or
suspicion of infectious etiology of exacerbation
 Consider adding IV Magnesium Sulphate if above treatments do not improve
symptoms
Consider noninvasive mechanical ventilation
 Evaluation may include chest radiograph, CBC with differential, basic metabolic
panel, ECG
 Address associated comorbidities

Indications for inpatient admission of COPD exacerbation patients

 Marked increase in intensity of symptoms, such as sudden development of resting
dyspnea or inability to walk from room to room
 Failure of exacerbation to respond to initial medical management
 Significant comorbidities
 Newly occurring dysrhythmias, heart failure
 Frequent exacerbations and/or frequent relapse after ED treatment
 Older age
 Insufficient home support
Indications for ICU care –
 Severe dyspnea that responds inadequately to initial emergency therapy
 Respiratory failure (current or impending) despite supplemental oxygen and
requirement of noninvasive positive-pressure ventilation
 Decreasing level of consciousness or increasing confusion or agitation
 Hemodynamic instability
 Presence of comorbidities leading to end-organ failure
Treatment of respiratory failure
Patients with emphysema may be at risk of hypercapnic respiratory failure and
acidaemiaduring acute illness, particularly if there is evidence of previous hypercapnic
respiratoryfailure.Monitor for signs of worsening CO2 retention (increased drowsiness,
reduced
cognitive function, headache).
Repeat ABG (on current FiO2) after 1 hour of therapy or if deterioration clinically.
 If PaCO2 < 6kPa consider prescribing target saturation range of 88-92% and maintain
with the lowest possible FiO2 via a controlled device (start at 24-28%).
 If pH >7.35 and PaCO2 > 6kPa prescribe target saturation range of 88-92% and
maintain with the lowest possible FiO2 via a controlled device (start at 24-28%).
 If pH < 7.35 and PaCO2 > 6kPa discuss patient with Consultant
Ensure adequate bronchodilator therapy.
Exclude and treat other causes of deterioration including LVF, cardiac ischaemia,
uncontrolled atrial fibrillation, pneumothorax, pulmonary embolism and hypovolaemia.
Indications for NIV (Refer NIV guidelines)
 Acidosis (pH <7.36)/hypercapnia (Paco2 >50 mm Hg)/
 oxygenation deficit (Pao2 <60 mm Hg or Sao2 <90%)
 Severe dyspnea with clinical signs like respiratory muscle fatigue
 or increased work of breathing
Exclusion criteria (any)
 Respiratory arrest
 Cardiovascular instability (hypotension, arrhythmias, myocardial infarction)
 Change in mental status; uncooperative patient
 High aspiration risk i.e Viscous or copious secretions
 Recent facial or gastroesophageal surgery
 Craniofacial trauma
 Fixed nasopharyngeal abnormalities
 Burns
 Extreme obesity
Discharge criteria
 The patient should be in a clinically stable condition and have had no need for
parenteral therapy for 24 hours
 Inhaled bronchodilators are required less than four-hourly
 Oxygen delivery has ceased for 24 hours (unless home oxygen is indicated)
 If previously able, the patient is ambulating safely and independently, and performing
activities of daily living.
 The patient is able to eat and sleep without significant episodes of dyspnoea
 The patient or caregiver understands and is able to administer medications
 Follow-up and home care arrangements have been completed.
NIV Guidelines(7,15,16)
There are two types of respiratory failure. Type 1 respiratory failure ischaracterized by
hypoxia without hypercapnia. Type 1 respiratory failuremay be the result of conditions that
affect oxygenation but not necessarilyventilation (e.g., pneumonia, pulmonary embolism).
Patients with type 1respiratory failure require assistance with oxygenation. Treatment of type
1failure focuses on optimizing oxygenation.
Type 2 respiratory failure ischaracterized by hypoxia with hypercapnia. Type 2 respiratory
failureis often the result of conditions that affect ventilation (e.g., chronicobstructive
pulmonary disease). Treatment of type 2 failure requires notonly optimizing oxygenation but
also supporting ventilation.
Noninvasive positive-pressure ventilation (NIPPV) provides positivepressureairway support
through a face or nasal mask without the useof an endotracheal tube or other airway device.
NIPPV is an initialnoninvasive airway management strategy. In adults, NIPPV includes
continuous positive airway pressure (CPAP) and bilevel positive airwaypressure (BiPAP).
Ideal patients forNIPPV are cooperative, have protective airway reflexes, and have intact
respiratory efforts. NIPPV is not appropriate in patients who have absentor agonal respiratory
effort, impaired or absent gag reflex, altered mentalstatus, severe maxillofacial trauma,
potential basilar skull fracture, life-threateningepistaxis, or bullous lung disease. Use NIPPV
with cautionin hypotensive patients because any volume depletion can be worsened
from the positive pressure, triggering more hypotension.
NIPPV reduces work of breathing through multiple mechanisms.NIPPV improves pulmonary
compliance and recruits and stabilizes collapsedalveoli, improving alveoli aeration and
ventilation-perfusionmismatches.1 NIPPV increases both intrathoracic and hydrostatic
pressure,shifting pulmonary edema into the vasculature. Increased intrathoracic
pressure can also decrease venous return, transmural pressure, andafterload, leading to
improved cardiac function. NIPPV also increasestidal volume and minute ventilation, leading
to increased Pao2 andreduction in Paco2. NIPPV reduces work of breathing by 60% and
dyspneascores by 29% to 67%, while improving inspiratory muscle endurance
by 14% to 95% over spontaneous respirations.
CPAP delivers a constant positive pressure throughout the respiratorycycle. BiPAP provides
different levels of positive airway pressure duringinspiration (inspiratory positive airway
pressure [IPAP]) and expiration(expiratory positive airway pressure [EPAP]). Although the
terms EPAPand positive end-expiratory pressure are often used interchangeably,
positive end-expiratory pressure is specific to the end of the respiratorycycle whereas EPAP
refers to the pressure administered via the BiPAPmachine during the entire expiratory phase.
Advantages
 Reduces work of breathing
 Improves pulmonary compliance
 Recruits atelectatic alveoli
 Less sedation
Disadvantages
 Air trapping
 Increased intrathoracic pressure
leading to decreased venous return,
afterload, and cardiac
 Abdominal compartment syndrome
 Shorter hospital stay
 Decreased rate of intubation
without risks of endotracheal
intubation
 output, and hypotension
 Pulmonary barotrauma leading to
pneumothorax
 Respiratory alkalosis

Typical starting settings for CPAP are 5 to 15 cm H2O.

Typical starting setting for BiPAP include ―spontaneous‖ mode with IPAP set to 8 to 10
cm H2O and EPAP set to 3 to 5 cm H2O.
Becautious when using NIPPV at pressures >15 cm H2O because this mayincrease the
intrathoracic pressure, leading to hypotension along withdecreased venous return, decreased
preload and afterload, and eventuallydecreased cardiac output.
Uses of NIVThe most common use of NIPPV is for cardiogenicpulmonary edemawhere
NIPPV may reduce rates of endotrachealintubation, hospital length of stay, and mortality.
In patientswith chronic obstructive pulmonary disease, NIPPV is helpful in those
with respiratory acidosis.
NIPPV may similarly benefit patients withmoderate to severe asthma exacerbations,
although data on effectivenessare limited.
Because of the bronchospastic nature of chronic obstructivepulmonary disease and asthma, be
vigilant for air trapping andsubsequent pneumothorax when using NIPPV.
NIPPV may reduce the rate of intubation and in-hospital death inpatients withpneumonia.
Exercise caution in this patient groupbecause hypovolemia may coexist, with resultant
NIPPV-inducedhypotension.
Management of Pneumonia(17)
When a diagnosis of community acquired pneumonia is made at presentation to hospital,
determine whether patients are at low, intermediate or high risk using the CURB65 score.
Use clinical judgement in conjunction with the CURB65 score to guide the management of
community-acquired pneumonia.
CURB65 score is calculated by giving 1 point for each of the following prognostic features:
 Confusion (New disorientation in person, place or time)
 Raised blood urea nitrogen (over 7 mmol/litre)
 Raised respiratory rate (30 breaths per minute or more)
 Low blood pressure (diastolic 60 mmHg or less, or systolic less than 90 mmHg)
 Age 65 years or more.
Patients are stratified for risk of death as follows:
 0 or 1: low risk (less than 3% mortality risk) – Consider home-based care for patients
 2: intermediate risk (3–15% mortality risk) – Consider hospital-based care for patients
 3 to 5: high risk (more than 15% mortality risk) – Consider ICU admission for
patients
Investigations –
 CBC
 RFTs
 CXR
 ECG
 ABG (If patient is tachypnoeic or Curb >2)
 Blood culture
Management –
Offer antibiotic therapy as soon as possible after diagnosis, and certainly within 4 hours to all
patients with community acquired pneumonia who are admitted to hospital.
Low-severity community-acquired pneumonia
Offer a 5-day course of a single antibiotic to patients with low-severity community-acquired
pneumonia. Consider amoxicillin in preference to a macrolide or a tetracycline for patients with
low-severity community-acquired pneumonia. Consider a macrolide or a tetracycline for patients
who are allergic to penicillin. Consider extending the course of the antibiotic for longer than 5
days as a possible management strategy for patients with low-severity community-acquired
pneumonia whose symptoms do not improve as expected after 3 days.
Explain danger signs to patients and care-givers about when to seek further medical advice - if
their symptoms do not begin to improve within 3 days of starting the antibiotic, or earlier if their
symptoms are worsening.
Do not offer patients with low-severity community-acquired pneumonia fluoroquinolones or dual
antibiotic therapy.
 Moderate- and high-severity community-acquired pneumonia
Consider a 7- to 10-day course of antibiotic therapy for patients with moderate- or high-severity
community-acquired pneumonia. Consider dual antibiotic therapy with amoxicillin and a
macrolide for patients with moderate-severity community-acquired pneumonia. Consider dual
antibiotic therapy with a beta-lactamase stable beta-lactam and a macrolide for patients with high-
severity community-acquired pneumonia.
Available beta-lactamase stable beta-lactams include: co-amoxiclav, cefotaxime,
ceftarolinefosamil, ceftriaxone, cefuroxime and piperacillin with tazobactam.
Hospital acquired Pneumonia
Offer antibiotic therapy as soon as possible after diagnosis, and certainly within 4 hours, to patients
with hospital acquired pneumonia. Choose antibiotic therapy in accordance with local hospital policy
(which should take into account knowledge of local microbial pathogens) and clinical circumstances
for patients with hospital-acquired pneumonia.
Consider a 5- to 10-day course of antibiotic therapy for patients with hospital-acquired pneumonia.

Pneumoniaseverity(based
onclinicaljudgementand Treatment Preferred treatment Alternativetreatment
CURB65) site

Low Home Amoxicillin500mg Doxycycline 200 mg

severity(eg,CURB65 =
0 to 1 or CRB65 score =
0,<3 percent mortality)
Moderateseverity (eg,
CURB65=2,9 percent
mortality)
orallythreetimesdaily loadingdose then 100
mgorallyoncedailyor
clarithromycin500
Hospital Amoxicillin 500mg to 1 Doxycycline 200 mg
mgorallytwicedaily
gram orally three loadingdose then 100
timesdailyplus mgorallyorlevofloxacin5
clarithromycin500mg 00mgorally
orallytwicedaily oncedailyormoxifloxacin

High severity(eg, Hospital Co-amoxiclav(amoxicillin- 400mgorally oncedaily¶

CURB65 = 3 to 5, 15 to clavulanate potassium) 1.2
40 percent mortality) gramsIVthreetimesdaily*
plus clarithromycin 500 mg
IV twice daily*
(IfLegionellastronglysuspecte OR Cefuroxime1.5
d,consider adding
levofloxacin Δ)
Benzylpenicillin(penicilli
nG)1.2gramsIV
fourtimesdailypluseitherle
vofloxacin500
mgIVtwicedaily
gramsIVthreetimesdaily
orcefotaxime1
gramIVthreetimesdaily
orceftriaxone2gramsIVon
cedaily,plus
clarithromycin 500 mg IV
Acute Kidney Injury(18,19)
Acute Kidney Injury (AKI) is a potentially reversible reduction in the capacity of the kidney
to excrete nitrogenous wastes and maintain fluid and electrolyte homoeostasis, which usually
occurs over hours to days. The initial clinical approach is identical in all patients—a thorough
history and examination with simultaneous treatment of any life threatening features (for
example, severe hyperkalaemia). Subsequent management should focus on determining the
cause, which may demand specific treatment, maintaining the patient‘s volume status, and
avoiding further nephrotoxic insults.
AcuteKidney Injurymaybeoliguric(urineoutputlessthan500mlin 24hrs)ornon
oliguric(urineoutputmorethan500ml/24hrs).
Suggestivefeatures
 Uremia– Drowsiness, nausea, hiccoughs. Can be associated with raisedBUNlevel.
 Raisedserumcreatinine
 Hyperkalemia
 Hyponatremia
 Metabolicacidosis
TheapproachtopatientswithAKIissimplifiedbyclassifyingitaspre –renal, intrinsicorpost–
obstructive
 Suspected Acute Kidney
Injury

A full drug history (current,

Treat any life threatening
recent, and alternative
features first—Stabilise ABCs,
medication) is vital. Is
Rule out shock, respiratory
this acute or chronic renal
failure, hyperkalaemia
impairment?

Is there a pre‐renal cause? Is intrinsic renal disease

What is the patient's Could this be obstruction? probable—what does
current fluid status? urine analysis show?

Assess the haemodynamic

status of the patient Examine for palpable Urinalysis should be done
Hypotension is usually easy bladder and look for past in all patients supspected
to spot—but can be h/o acute retention to have ARF
relative.*

If present catheterise Haematuria, Proteinuria,

Check JVP and postural casts are suggestive of
hypotension patient and send urine
routine intrinsic renal disease

If volume is depleted -
Replace with small rapid
infusions of 200-250ml
crystalloid with regular
reassessment
If bladder not palpable, Admit for further
consider Ultrasonography evaluation of Renal disease
to rule out obstruction and ARF

Investigations to be sent –
 Urinalysis, Urine osmolality, Urine Sodium
 CBC
 RFTs – Creat and Urea, Na, K, Ca, PO4
 ABG/VBG
 Blood/Urine culture (if infection suspected)
 ECG, CXR
 Ultrasound – Abdomen and Pelvis

Admission Criteria – Indications for Dialysis

 Unstable vitals  Severe hyperkalaemia, unresponsive to
 Dehydration medical therapy
 Pulmonary oedema  Fluid overload with pulmonary oedema
 Features of Uremia/Elevated Creatinine  Uraemic Complications -Encephalopathy,
 Metabolic Acidosis pericarditis, neuropathy/myopathy
 Hyperkalemia  Severe acidosis (pH <7.1)
 Anuria  Drug overdose with a dialysable toxin
 Drug overdose
*Relative Hypotension – A systolic pressure of 110 mm Hg in the hypertensive patient whose normal value is
around 160 mm Hg can compromise renal perfusion.

Difference B/w Pre-

renal and Renal??
Treatment and Disposition –
Management is directed at treating any life threatening features, attempting to halt or reverse
the decline in renal function, and if unsuccessful providing support by renal replacement
anticipating renal recovery. Hyperkalaemia, pulmonary oedema, and severe acidosis require
immediate attention.
Fluid balance, the treatment of less severe acidosis, the use of diuretics and dopamine, as well
as the relief of obstruction are all issues in the further management of the patient—some
more controversial than others.
Provided the patient can be maintained through the period of non‐function, and no further
insults accrue, the kidney is remarkable in its ability to recover its normal homoeostatic role.
1) Hyperkalaemia
Severe hyperkalaemia (plasma potassium (K+>6.5 mmol/l) is a medical emergency because
of the risk of life threatening cardiac arrhythmias. As K+ rises, a typical pattern of ECG
changes ensues: peaked/tented T waves ([K+]p>6.5 mmol/l); flattening of the P wave and
prolongation of the QRS complex ([K+]p 7–8 mmol/l); sine waves ([K+]p 8–9 mmol/l); and
ventricular fibrillation or asystole ([K+]p >9 mmol/l)13 (fig 44).). These changes are not
always consistent, however, and patients with a normal baseline ECG may also develop
arrhythmias. Urgent treatment of hyperkalaemia should be started if the serum potassium is
>6.5 mmol/l, or if any ECG changes are present.

An ECG from a haemodialysis patient with a serum potassium of 8.0 mmol/l, showing the classic changes of
significant hyperkalaemia: tented T waves, flattening of the P wave, and prolongation of the QRS complex.
Summary of treatment strategies in hyperkalaemia (see text for references)
Treatment Time to Action Reduction in [K+]p Duration of action

Calcium gluconate/carbonate 1–3 min Nil 30–60 min

Insulin (+/− dextrose) 15–30 min 0.65–1.0 mmol/l 4–6 h

Salbutamol (nebulised) 30 min* 0.6–1.0 mmol/l 2–4 h

Ion exchange resin 2–3 h 0.5–1.0 mmol/1 g resin 4–6 h

Haemodialysis Immediate ⩽1.5 mmol/l/h While dialysis ongoing

 a) Stabilisation of cardiac myocyte
Calcium antagonises the effects of hyperkalaemia, stabilising the myocardium within a few
minutes of infusion and producing a more normal ECG trace without affecting serum
potassium. It should be given immediately if P wave or QRS changes are present. A bolus of
10ml of 10% calcium gluconate or chloride is given intravenously over two to five minutes—
the former is preferable because of a lower risk of tissue damage if extravasation occurs.
b) Reduction in plasma potassium concentration
Treatment with calcium is a temporising measure ―buying time‖ while measures are started to
reduce the serum potassium through increasing cellular uptake. Various options exist:
i) Insulin with glucose
Insulin acts rapidly to indirectly activate the cell membrane Na+/K+−ATPase and
thus increase cellular potassium uptake, probably via activation of Na+/H+ channels
and an increase in intracellular [Na+]. The addition of glucose to the insulin bolus is
necessary to prevent hypoglycaemia. Ten units of fast acting soluble insulin should be
added to 50 ml of 50% dextrose and infused over 10–20 minutes. A reduction in K+ is
seen after 20–30 minutes. Insulin alone can be given to hyperglycaemic patients
(blood glucose >14 mmol/l) as the infusion of further glucose can worsen
hyperkalaemia secondary to its osmotic effect. Whether insulin and dextrose, or
insulin alone, is used, the blood glucose should be monitored carefully for at least six
hours. Hypoglycaemia occurred in up to 75% of patients in some studies, and was
generally associated with higher insulin or lower glucose doses.13
ii) β2 adrenergic agonists
Salbutamol binds to β2 receptors and through cytosolic second messengers activates
the Na+/K+−ATPase, thus promoting cellular potassium uptake. Nebulised and
intravenous salbutamol produce a similar effect to insulin, but at higher doses than
used for bronchospasm (10–20 mg via nebuliser, or 0.5 mg intravenously). Up to 40%
of patients do not respond. Tachycardia is common especially after intravenous
administration. The method should not be used in patients taking β blockers or in
those with a high risk of cardiac side effects. For these reasons, insulin is the agent of
choice to reduce [K+]p, but salbutamol may be preferably in certain circumstances,
especially paediatric patients,18 and combined therapy with insulin and dextrose plus
salbutamol may be more effective than either treatment alone.
Sodium bicarbonateThe infusion of sodium bicarbonate has little immediate effect on
hyperkalaemia, but may be used to correct acidosis (see later).
c) Removal of potassium from the body
While the above techniques serve to redistribute potassium, the overall amount retained by a
patient with ARF will still be excessive and encouragement of potassium loss is often needed.
 i) Ion exchange resins
These bind potassium in the GI tract, in exchange for calcium or sodium, and result in
increased potassium excretion in the stool. Calcium resonium (calcium polystyrene
sulphonate) and Resonium A (sodium polystyrene sulphate) are the most commonly
used, given at an oral dose of 15 g up to thrice daily, together with an osmotic laxative
(for example, lactulose 10 ml) to prevent constipation. They can also be given
rectally. An effect takes two to three hours. Side effects include hypercalcaemia and
salt/water overload (with calcium and sodium containing resins respectively), and
hypomagnesaemia.
d) Haemodialysis
This is the definitive means by which potassium can be removed from the body, and is
indicated in refractory severe hyperkalaemia. Haemodialysis is more effective than
haemofiltration or peritoneal dialysis at potassium removal and has an immediate effect once
started. Maximum removal occurs in the first hour of dialysis.
e) Prevention of further potassium accumulation.
This can be achieved through a low potassium diet.
2) Pulmonary oedema
Pulmonary oedema is often the result of excessive fluid resuscitation, and can be anticipated
in many patients—especially those with known cardiac dysfunction and can be avoided by
more judicious intravenous fluid therapy. The oligo‐anuric patient with pulmonary oedema
resulting from fluid overload (with/without underlying cardiac disease) represents a clinical
challenge. If significant respiratory failure is present, this must be dealt with first, through
supplementary oxygen, NIV or intubation and ventilation, depending on the state of the
patient. The main indication for use of diuretics is management of volume overload. Iv loop
diuretics, as a bolus or continuous infusion, can be used. However, it is important to note that
they do not improve morbidity, mortality, or renal outcomes, and should not be used to treat
in the absence of volume overload.If these interventions are not successful, then fluid
removal by renal replacement therapy is the definitive answer.
3) Acidosis
Severe metabolic acidosis (blood pH <7.2) often accompanies AKI and arises through a
variety of mechanisms, related both to reduced renal function and the underlying cause of the
patient‘s illness. Systemic acidosis impairs cardiac contractility, induces bradycardia,
produces vasodilatation, and augments hyperkalaemia, among other effects. Reversing
acidosis through administration of an alkaline solution—sodium bicarbonate—would seem to
be sensible, but there is very little evidence to show that it provides benefit. Bolus therapy
with hypertonic (8.4%) sodium bicarbonate can worsen intracellular acidosis (while
deceiving the clinician through improving blood pH—paradoxical acidosis) and cause
osmotic vasodilatation, overshoot metabolic alkalosis, hypernatraemia, and
extravasation injury if not delivered into a central vein.Isotonic (1.26%) solutions may
have a role as fluid replacement therapy in stable patients with a moderate to severe acidosis
and a requirement for fluid replacement, in whom dialysis is not imminent. Haemodialysis or
haemofiltration will usually be required to treat severe acidosis in oligoanuric patients.
4) Fluid balance
The approach to the hypovolaemic patient with pre‐renal failure has been described earlier.
Which is the optimal resuscitation fluid is still debated. Normal saline and 4% albumin have
clinical equivalence, shown by the recent SAFE study of patients admitted to intensive care
units in Australia and New Zealand, and which overturns previous studies showing that
albumin use may be associated with a higher mortality.Once the patient is considered
euvolaemic (normotensive, no postural drop, JVP and/or central venous pressure (CVP)
normal), care should be taken to avoid fluid overload and a maintenance regimen started,
which takes account of renal and insensible losses, aiming for a positive balance of 500
ml/day. This requires accurate observation and record keeping by nursing staff, and regular
re‐assessment by the clinician.
5) Dopamine
The use of low dose (1–3 μg/kg/min) dopamine has been advocated to increase renal
perfusion in critically ill patients. Recent studies, have shown a lack of efficacy on renal
outcome or overall mortality.22,23 Its routine use in ARF is not currently justifiable.
6) Diuretics
There is a theoretical rationale for the use of loop diuretics in ARF—inhibition of the
Na+/K+/2Cl− pump in the thick ascending limb of the loop of Henle, with subsequent
decrease in Na+/K+−ATPase activity, should reduce the oxygen requirements of these cells,
and thus their susceptibility to ischaemic damage.There are scarce clinical data to support
this, and recent studies have either correlated the use of diuretics with increased mortality,2 or
shown no benefit. Converting oliguric to non‐oliguric renal failure may help with fluid and
electrolyte management, but does not seem to affect eventual need for dialysis or overall
mortality, and should not delay the start of renal replacement therapy when otherwise
indicated.There are no data to support the use of mannitol.
7) Relief of obstruction
It is important to relieve urinary tract obstruction promptly. Bladder outflow obstruction can
be relieved by passage of a urethral catheter—which should be considered in all patients with
AKI to accurately measure urine output—but relief of upper tract obstruction may require
either antegrade (percutaneous nephrostomy) or retrograde (cystoscopy and retrograde
ureteral catheterisation) approaches. Urethral catheterisation can be performed immediately,
but other techniques require planning. Close collaboration between nephrological, urological,
and radiological services is required, and in many cases renal replacement therapy may be
necessary before relief of obstruction can be achieved.
8) General measures
In addition to the specific measures discussed above, the ongoing care of the patient with
AKI should be directed at preventing further renal insults and supporting normal physiology.
Additional renal damage is often accrued through recurrent episodes of reduced renal
perfusion, sometimes difficult to avoid in the unstable patient, but also through the
administration of nephrotoxic drugs, most often NSAIDs, ACE‐I, and aminoglycoside
antibiotics. There are many other drugs that require dose adjustment depending on the
patient‘s GFR, not because they are directly nephrotoxic, but because impaired renal
excretion changes their pharmacodynamics (for example, cephalosporin antibiotics,
morphine). The use of contrast media should also be avoided. Patients with AKI may suffer
from excessive bleeding, because of uraemia induced platelet dysfunction and coagulopathies
(for example, sepsis associated disseminated intravascular coagulation). Correction of
coagulopathy may be necessary with blood products and vitamin K. There is an increased
susceptibility to infection. Good infection control practices and a low threshold for
considering an infectious aetiology for any clinical deterioration may minimise the risk. Care
of pressure areas and prophylaxis against deep venous thrombosis can avoid some of the
problems of prolonged immobility.
The Altered Sensorium Patient – Unconsciousness, Syncope, Confusion
Aetiology of Unconsciousness -
 Traumatic brain injuries - Trauma due to road traffic, fall, violence, blasts injuries.
 Stroke - Subarachoid Hemorrhage, intracerebral massive bleed, or major vessel
occlusion or massive brain oedema and coning.
 Diabetes Mellitus - Hypoglycemia (acute onset coma) and hyperglycemia.
 Uremia – Sub acute onset of loss of consciousness, with obvious history.
 Hypoxia - Drowning of post CPR.
 Infections. Encephalitis and meningitis. Toxemia, Septicemia.
 Seizures. Status epilepticus, post ictal coma,
 Toxins. Carbon monoxide, organophosphorous compounds or lead,
 Tumors of the brain - Sudden bleeding within the tumor causing acute swelling,
massive brain oedema and coning of brainstem.
 Alcohol – Acute alcoholic intoxication results in coma.
 Drugs - Marijuana, opioids
Ensure to check GRBS for all patients with altered sensorium.

Don’t Forget to
Check GRBS
Approach to Altered Sensorium
Seizures in an Adult(7)
 Treatment of Active seizures -
Typically, little is required during the course of an active seizure otherthan supportive and
patient protective measures. If possible, turn thepatient to the side to reduce the risk of
aspiration. It is usually not necessaryor even possible to ventilate a patient effectively during
a seizure,but once the attack subsides, clear the airway. Suction and airwayadjuncts should be
readily available. It is not necessary or recommendedto give IV anticonvulsant
medications during the course ofan uncomplicated seizure. Most seizures will self-resolve
within5 minutes. Any unnecessary sedation at this point will complicate the
evaluation and result in a prolonged decrease in level of consciousness.Seizures that fail to
abate after 5 minutes are considered status epilepticusand require more aggressive medical
interventions (see ―StatusEpilepticus‖ section, below).
 Treatment of patient with history of Seizures
Proper management of a patient with a well-documented seizure disorderwho presents after
one or more seizures depends on the particularcircumstances of the case. Identify and correct
potential precipitants thatmay lower the seizure threshold. Many seizures occur because of
failureto take anticonvulsant medication as prescribed. If anticonvulsant levels are verylow,
supplemental doses are appropriate, and the regular regimen can berestarted or adjusted. A
loading dose is also frequently provided. Withouta loading dose, the patient may not achieve
anticonvulsant effects fordays to weeks and is at risk for subsequent seizures. If the
maintenance doseis increased, ensure follow-up within 1 to 3 days. There are no
specificguidelines for the duration of ED observation in the situation of an individualwith a
prior history of seizures. Some clinicians discharge patientswith seizures resulting from
nontherapeutic anticonvulsant levels afteradministration of a loading dose of an
anticonvulsant if vital signs arenormal and the mental status has returned to baseline. Ideally,
dischargepatients with a family member or friend and with follow-up arranged.
 SPECIAL POPULATIONS
 HUMAN IMMUNODEFICIENCY VIRUS
Mass lesions, encephalopathy, HZV, toxoplasmosis, Cryptococcus,neurosyphilis, and
meningitis are all seen more frequently in thispopulation and can all provoke seizure
activity.Perform an extensive investigation for the cause of the seizure. If nospace-occupying
lesion is identified on non-contrast head CT scan andthere is no evidence of increased
intracranial pressure, perform a LP to exclude CNS infection. If no explanation for seizures
isfound, then obtain a contrast-enhanced head CT or MRI. These patients need to be admitted
for further evaluation
  NEUROCYSTICERCOSIS
Neurocysticercosis is caused by a CNS infection with the larval stage ofthe tapeworm Taenia
soliumand is the most common cause of provoked(secondary) seizures in the developing
world. The most common formof disease is parasitic invasion of brain parenchyma and cyst
formation.Over 1 to 2 years, the cyst degenerates and becomes fibrotic, leaving afocal area of
scar and calcification. Seizures are the most commonclinical manifestation of
neurocysticercosis and most frequently occuras the parasite is degenerating. In 80% to 90%
of cases, the lesionsresolve within 3 to 6 months, leaving the patient free of seizures. Up to
20% of patients will continue to have seizures and require ongoingtherapy with antiepileptic
medications.In most cases, neuroimaging in neurocysticercosis is nondiagnostic.CT or MRI
may demonstrate a 1- to 2-cm cystic lesion with thin walls, a localized area of
ringlikeenhancement with surrounding edema, a calcified lesion, or hydrocephalus.Definitive
diagnosis relies on a combination of the patient‘sclinical picture, exposure history, serologic
testing, and neuroimaging.Seizures in NCT are typically controlled by
antiepilepticmonotherapy. Definitive treatment of neurocysticercosis is controversialand
highly variable, depending on the number, location, andviability of the parasites within the
CNS. Antiparasitics (praziquanteland albendazole) and steroids are best initiated in
consultation with a neurologist.
 PREGNANCY
The management of seizures during pregnancyrequires a multidisciplinary approach. Most
seizures in pregnancy arenot first-time seizures, and initial evaluation is generally as
discussedearlier, with the addition of an obstetric evaluation to determine gestationalage and
fetal well-being.When a woman beyond 20 weeks of gestation develops seizures inthe
setting of hypertension, edema, and proteinuria, the condition isdefined as eclampsia.
Magnesium sulfate has long been used to treateclampsia with good results. Detailed
discussionof seizures in pregnancy is discussed in The OBG Care Pathway.
 ALCOHOL ABUSE
Seizures and alcohol use are associated through missed doses of medication,sleep deprivation
as an epileptogenic trigger, increased propensityfor head injury, toxic co-ingestions,
electrolyte abnormalities, and withdrawalseizures. Benzodiazepines in doses sufficient to
manage withdrawalsymptoms will usually afford adequate protection from acuteseizures.
These doses are often very large and need to be given in anescalating fashion. Evaluate and
treat the alcohol-abusing patient as any other patient with a first-time seizure. The patient will
require admission, monitoring, thiamine infusions and GRBS monitoring.
Status Epilepticus
Defn - Status epilepticus is a single seizure ≥5 minutes in length or two or more seizures
without recovery of consciousness between seizures.
Algorithm for management of Status epilepticus
 Intracranial Pressure(20,21)

Raised intracranial pressure (ICP) can arise as a consequence of intracranial mass lesions,
disorders of cerebrospinal fluid (CSF) circulation and more diffuse intracranial pathological
processes. Its development may be acute or chronic. Normal values for ICP increase with
age, from approximately 6 mm Hg in infants to 10 to 15 mm Hg in adults
Increased ICP may cause cerebral ischemia by directly decreasing cerebral perfusion pressure
and hence cerebral blood flow (CBF) to critical levels in keeping with the equation:
Cerebral Perfusion Pressure = Mean Arterial Pressure - Intracranial Pressure
Aetiology
 Localised mass lesions: traumatic haematomas (extradural, subdural, intracerebral).
 Neoplasms: glioma, meningioma, metastasis.
 Abscess.
 Focal oedema secondary to trauma, infarction, tumour.
 Disturbance of CSF circulation: obstructive hydrocephalus, communicating hydrocephalus.
 Obstruction to major venous sinuses: depressed fractures overlying major venous
sinuses, cerebral venous thrombosis.
 Diffuse brain oedema or swelling: encephalitis, meningitis, diffuse injury, subarachnoid
haemorrhage, Reye's syndrome, lead encephalopathy, water intoxication, near drowning.
 Idiopathic intracranial hypertension.
Presentation
The combination of headache, papilloedema and vomiting is generally considered indicative
of ICP -
 Headache: more worrying when nocturnal, starting when waking, worse on coughing or
moving head and associated with altered mental state.
 Early changes in mental state include lethargy, irritability, slow decision making and
abnormal social behaviour. Untreated, this can deteriorate to stupor, coma and death.
 Vomiting, which can progress to projectile with rising ICP.
 Pupillary changes, including irregularity or dilatation in one eye.
 Fundoscopy shows blurring of the disc margins, loss of venous pulsations, disc hyperaemia
and flame-shaped haemorrhages. In later stages, obscured disc margins and retinal
haemorrhages may be seen.
 Unilateral ptosis or third and sixth nerve palsies. In later stages, ophthalmoplegia and loss
of vestibulo-ocular reflexes.
 Late signs include motor changes (hemiparesis), raised blood pressure, widened pulse
pressure and slow irregular pulse.
 Acute situations:
  Head injury and obtundation: bleeding can form a rapidly expanding haematoma
leading to rapidly rising ICP if not treated promptly.
 Syncope, headache and meningismus: abrupt onset of headache with these symptoms
suggests ruptured cerebral aneurysm or vascular lesion.
 Focal deficit followed by seizures: focal deficit can be associated with a mass lesion
and when there is oedema or haemorrhage. Intracranial compartment shift can cause
increased ICP within minutes or hours; status epilepticus can cause decompensation
of cerebral volume regulation.
 'Talk and deteriorate': patients typically talk recognisably following head injury, then
go into coma in the first two days. The usual cause is an intracranial haematoma.
Investigations
 CT/MRI scanning to determine any underlying lesion.
 Check and monitor blood glucose, renal function, electrolytes and osmolality.
Management
Initial Resuscitation - A primary assessment of airway, breathing, and circulation must be
completed for all patients presenting with potential neurological insults. It is imperative that
prompt treatment of the major aggravators of secondary injury, particularly hypotension and
hypoxemia, be administered. Airway protection must be ensured for patients with an altered
level of consciousness. Patients with a GCS score less than 8 require invasive airway support.
Normal oxygenation and ventilation must be maintained (oxygen saturation, 995%; PaCO2 ,
35Y40 mm Hg). Poor ventilation resulting in hypercarbia (PaCO2 , 945 mm Hg) causes
cerebral vasodilation and a secondary increase in ICP. Maintenance of a systolic blood
pressure greater than the fifth percentile for age is essential. Hypotension during the initial
resuscitation is the most critical factor influencing survival for patients with traumatic brain
injury. Hypotension requires aggressive fluid resuscitation with crystalloids because there is a
greater association between poor neurological outcome and hypotension occurring in the first
6 hours after traumatic brain injury than with hypotension at any other time during recovery.
In the acute emergency situation the priority is maintaining adequate arterial oxygen tension
and ensuring normal vascular volume and normal osmosis. It is also essential to maintain
normoglycaemia. Otherwise, treatment will depend on the underlying pathology.
First-line therapies
 Avoid pyrexia: this increases ICP and is an independent predictor of poor outcome.
 Manage seizures: they contribute to raised ICP and should be managed aggressively using
standard anticonvulsant loading regimens.
 Head of bed elevation: elevating the head of the bed to 30° improves jugular venous
outflow and lowers ICP. In patients who are hypovolaemic, this may be associated with a
fall in blood pressure and an overall fall in cerebral perfusion pressure.
 Analgesia and sedation: usually with intravenous propofol, etomidate or midazolam for
sedation and morphine or alfentanil for analgesia and antitussive effect.
 Neuromuscular blockade: muscle activity may further raise ICP by increasing
intrathoracic pressure and obstructing cerebral venous outflow. If this does not respond to
analgesia and sedation then neuromuscular blockade is considered.
 Mannitol (an intravascular osmotic agent):
 The typical dosage is 0.25 to 1 g/kg of 20% mannitol given over 10 to 20 minutes.
 The major problems associated with mannitol are hypovolaemia and the induction of
a hyperosmotic state.
 Serum osmolality should not be allowed to rise over 320 mOsm/kg.
 Mannitol therapy for raised ICP may have a beneficial effect on mortality when
compared with pentobarbital treatment but may have a detrimental effect on mortality
when compared with hypertonic saline.
 Hypertonic saline 3-30% has been shown to be effective in patients with raised ICP
following a stroke when mannitol has been ineffective.
 The typical dosage is 5 to 10 mL/kg of 3% hypertonic saline solution given over 5 to
10 minutes.
Hyperventilation: this lowers ICP by inducing hypocapnoeic vasoconstriction and
has been shown to be effective in reducing raised ICP. However, hyperventilation also
induces or exacerbates cerebral ischaemia in a proportion of patients. Prophylactic
ventilation with hyperventilation for patients with head injury has not been shown to
produce any benefit one year after injury. Maintain pCO2 at around 35mm
Second-line therapies
 Optimised hyperventilation: this involves the use of more aggressive hyperventilation,
with measurement of jugular venous saturation in an attempt to prevent hyperventilation-
induced ischaemia. The main problem with this approach is that focal areas of cerebral
ischaemia may be produced even though global measures suggest adequate oxygen supply.
 Hypothermia: cooling to 35°C (rather than 33°C) is effective in lowering refractory
intracranial hypertension and has fewer systemic complications in, for example, the
pulmonary system, infections, coagulation and electrolytes. There appears to be a
significant rebound in ICP when induced hypothermia is reversed.
 Decompressive craniectomy: this technique has been reported as being beneficial in head
injury, cerebral infarction, spontaneous intracerebral and subarachnoid haemorrhage. There
is no evidence to support the routine use of secondary decompression craniectomy to
reduce unfavourable outcome in adults with severe traumatic brain injury and refractory
high ICP. However, decompression craniectomy may be a useful option when medical
treatment has failed to control ICP.
 Poisoning – General Approach and Specific Drug Ingestions(7,22–26)

General Approach –
For effective management of an acutely poisoned victim, five complementary steps are
required. These are :
1. Resuscitation and initial stabilization
2. Diagnosis of type of poision
3. Nonspecific therapy
4. Specific therapy
5. Supportive care
1. Emergency Management Resuscitation and Stabilization: On first contact with the
patient, assessment of the level of consciousness is important. For an unconscious patient,
carefully evaluate ABC, followed by active measures to not only secure these, but also to
reverse the unconscious state, if possible. Important to look for obvious associated trauma.
 A – Airway: A patent airway is critical in the further management of the patient.
The following measures may maintain patency, if the patient is unconscious –
o The head tilt, chin lift technique or the classical jaw thrust would be the
initial method of choice. However, in the event that a neck trauma is
suspected, the head tilt should not be employed. The modified jaw thrust is
an alternative technique that may be employed in traumatized patients.
o Insertion of oro-pharyngeal / naso-pharyngeal airway with regular
suctioning. Prior to this the oral cavity should be inspected and any
obvious foreign bodies such as or broken dentures should be removed.
o Turn the patient to the recovery (three quarters prone) position. This
allows oral secretions and vomitus in the oropharynx to drain out.
o Endotracheal or nasotracheal intubation. If performed, this should be only
with a cuffed tube.
o Surgical cricothyrotomy Examination of the airway is not complete
without evaluating for the presence or absence of the gag reflex. Especially
in the unconscious patient, the absence of the gag reflex mandates
definitive measures to protect the airway, such as with a cuffed
endotracheal tube before any GI decontamination is instituted.
 B- Breathing: Assessment of breathing should include not just whether the
patient is breathing, but also if the breathing is slow or fast. Any patient with
abnormal breathing should be provided with 100% oxygen and assisted
ventilation, if required either via a bag-valve mask or positive pressure ventilation,
may be instituted.
  C- Circulation: Assessment of circulation should include HR, BP, peripheral
circulation and hydration status of the patient. To maintain the circulation,
o IV Fluids – Crystalloids, colloids – may be necessary
o Dopamine and Dobutamine may be needed to maintain the BP
o CVP monitoring may be necessary
o ECG monitoring may be needed
o If in shock, the patient should be maintained in a head-down position
Other problems
The patient may also have other problems like altered sensorium, seizures, etc.
Resuscitation is the first priority in any poisoned patient. After resuscitation, a structured
risk assessment is used to identify patients who may benefit from an antidote,
decontamination, or enhanced elimination techniques. Most patients only require provision of
good supportive care during a period of observation in an appropriate environment.
IV crystalloid bolus (10 to 20 mL/kg) is first-line treatment of hypotension. Since most
patients without toxin-induced fluid loss are generally not fluid depleted, avoid
administration of excess fluid.
Once ABCs are stabilised, attempt to establish the toxidrome that the patient belongs to. The
substance consumed is at times apparent but at other times is an unknown compound or a
mixture of substances. An approach that can be used in such situations is outlined below –

2. Clinical Evaluation (Identification of toxin/toxidrome)

 History
i. The primary aims of taking the history (can be taken when the patient‘s
condition is stable )are to
ii. Confirm that poisoning has occurred and identify the substance involved
iii. Always remember – All poisonings are Medico-legal cases.
 Physical Examination
i. Vitals – Pulse, BP, RR, Temperature, GRBS, spO2 and GCS
ii. Pupils – Size, Symmetry and reactivity, Nystagmus, papilloedema
iii. Head to Toe Examination –
a. Hydration status
b. Skin changes – Redness, moistness, dry
c. Needle track marks
d. Self harm marks
e. Odour of Breath
iv. Systemic Examination – Detailed systemic examination targeted towards
identifying toxidrome that patient belongs to.
Algorithm of Identifying Toxidrome
Investigations – Send general investigations for all patients but send targeted tests based on
clinical features and toxidromes.
One or more of the following samples can be sent for toxicology
 Blood
 Urine
 Gastric aspirate
 Other tests for initial management ( as required) – Serum digoxin levels, Serum
phenytoin levels, serum paracetamol levels
Effects of the agent
A number of different investigations may be necessary for evaluating the effects of the
poison.
 CBC, RFTs
 PT, PTT
 LFT – for hepato-toxic drugs
 ABG
 Urine routine and microscopy
 ECG
 Chest X- Ray
 Magnesium, calcium, phosphate levels
 Blood grouping and cross matching for fresh frozen plasma
 CPK levels
 Meth-hemoglobin
 Serum cholinesterase levels
 Serum osmolality for toxic alcohols
Attempt to identify the toxin by calling manufacturer, asking relatives to buy another pack of
the same poison; any clue can aid management of the patient.
3. Non Specific Management -
 Secure ABCs of the patient
 Decontamination
o Decontamination is the process of preventing systemic absorption into the
body. In the case of ocular or dermal exposure, this is achieved by copious
irrigation with water, after removal of contaminated clothing to expose the
area. Water irrigation is not used for metallic potassium, magnesium, or
sodium because these can ignite on contact with water. Instead, in these very
rare exposures, the area should be covered with petroleum jelly or mineral oil.

 Gastric Lavage –
 o Gastric lavage, the process of directly removing an ingested substance from
the stomach using a 30 Fr or larger orogastric tube, also has little data or
evidence showing its efficacy and should not be performed routinely for the
treatment of poisoned patients. Given the risks of aspiration and esophageal
trauma, the American Association of Poison Centers suggests it only be
employed ―within an hour of ingestion of a potentially life-threatening poison
which does not adsorb to activated charcoal or for which no antidote exists‖
and, even then, in a center with ―sufficient expertise‖ to perform the procedure
safely. Only a rare overdose will meet all these criteria; and hence, despite its
once widespread use, gastric lavage is mostly of historical interest only.
 Activated charcoal -
o Historically, single-dose activated charcoal (SDAC) has been the mainstay of
gastric decontamination in medical toxicology. Activated charcoal is a
carbonaceous substance that has been exposed to high heat and steam,
resulting in a large surface area to volume ratio, to provide ample surface
space for ingested substances to adsorb, and thus decrease absorption into the
body. Its use is recommended in certain overdose scenarios. Benefits include
decreasing primary absorption, or binding during enterohepatic recirculation
of a potentially toxic xenobiotic. These benefits are more likely to occur if:
 The activated charcoal is administered within one hour post-ingestion,
 The patient is alert, able, and willing to cooperate with administration,
and anticipated to remain alert and protective of airway reflexes.
 There is evidence of a massive ingestion of a toxic agent
 If the patient is sedated, has an unprotected airway, or is unwilling to
drink the charcoal suspension, administration is contraindicated. This
may be particularly true for young children.
 Activated charcoal (SDAC) – 1g/kg ≈50-60g per nasogastric tube.
o Potentially Lethal Toxins Where Early ActivatedCharcoal May Be
Indicated –
o Cyanide
o Colchicine
o Calcium channel blockers
o Cyclic antidepressants
o Cardio glycosides
o Cyclopeptide mushrooms (Amanita phalloides)
o Cocaine
o Cicutoxin (water hemlock)
o Salicylates
 Substances That Do Not Bind to
Activated Charcoal -
Pesticides
Heavy metals
Acids/alkalis
Iron
Lithium
Solvents

 Multiple Doses Activated Charcoal –

Unlike preventing absorption of a drug as is the case for SDAC,MDAC is intended also to
facilitate removal of a toxin that hasalready been absorbed. MDAC decreases xenobiotic
absorptionand elimination half-life when large amounts of the toxin areingested and
dissolution is delayed (eg, concretions, bezoars, orextended release formulations)
MDAC interferes with reabsorption of drugs that have entero-hepatic circulation by binding
them duringtheir transit of the gastrointestinal tract. As with SDAC,MDAC administration
may cause pulmonary aspiration andintestinal obstruction. Aspiration is best avoided by
applying thesame conditions for administration as for SDAC—ie, patient
awake, alert, and cooperating and is anticipated to remain awakeand alert. Obstruction is
more difficult to predict and prevent,although avoidance in situations with delayed gut
motility (eg,critical illness, opioid or anticholinergic effects) is recommendedto reduce this
risk.When MDAC is indicated, the initial loading dose of anactivated charcoal–to-xenobiotic
ratio of 10 : 1, is followed by subsequent doses of 50% of the initial dose every 4 to 6 hours
forup to 24 hours.MDAC may be discontinued when the patient‘smeasureable serum levels
are no longer considered in the toxicrange.
Specific Measures –
Toxin Antidote
Acetaminophen N-Acetylcysteine
Benzodiazepines Flumazenil
Carbamates Atropine
Digitalis glycosides (digoxin, digitoxin, oleander) Digoxin-specific Fab fragments
Ethylene glycol Ethanol
Methanol Ethanol
Opioids Naloxone
Organophosphates Atropine, Pralidoxime
Tricyclic antidepressants NaHCO3

Acetaminophen Poisoning(27–29)
Acetaminophen (better known internationally as paracetamol) is one of the most important
toxins encountered in emergency care because of its ready availability, high lethality, and
absence of clinical indications of ingestion until the time to administer the effective antidote
has passed. Acetaminophen is found as an isolated product or in combination medications for
the treatment of pain and febrile illness. Acetaminophen is absorbed rapidly, with peak
plasma concentrations generally occurring within 1 hour and complete absorption within 4
hours. Once absorbed, acetaminophen inhibits prostaglandin E2 (PGE2) synthesis, leading to
antipyresis and analgesia. Inhibition of PGE2 synthesis is either by direct cyclooxygenase-2
(COX-2) inhibition or inhibition of membrane associated prostaglandin synthase.
Clinical Features -
Early after acute acetaminophen ingestion, patients may beasymptomatic or have mild
nonspecific symptoms (Eg, nausea,vomiting, anorexia, malaise, and diaphoresis). Liverinjury
becomes evident after a period of 8 to 36 hours as an elevationin AST.Once liver injury
hasbegun, patients may develop right upper quadrant (RUQ) pain ortenderness, vomiting, and
jaundice. AST concentrations continueto rise rapidly and usually peak in 2 to 4 days,
corresponding tomaximal liver injury.ALT, prothrombintime (PT), and bilirubin typically
begin to rise and peak severalhours after AST values. With severe toxicity, AST, ALT, and
the PTmay all be elevated within 24 hours. With maximalliver injury, patients develop signs
and symptoms consistent withfulminant liver failure, including metabolic acidosis,
coagulopathy and hepatic encephalopathy. Death occurs from hemorrhage,adult respiratory
distress syndrome, sepsis, multiorganfailure, or cerebral edema. The risk of renal injury
increases with the severity of hepatic injury, occurringin less than 2% of patients without
hepatotoxicity and in 25% ofpatients with severe hepatotoxicity.
If patients recover, aminotransferases return to baseline concentrationsover a 5- to 7-day
period, althoughcomplete histologic resolution of liver injury may take months.Once
histologic recovery is complete, there are no long-termsequelae to the liver and patients are
not at risk for chronic hepaticdysfunction.

The goals of patient assessment after acetaminophen ingestion are -

(1) The determination of the patient‘s risk
(2) Diagnostic testing,
(3) Treatment with the antidote NAC when appropriate.

Rumack-Matthew
Normogram
 In an adult patient, significantly greater than 10 grams in total or 150 mg/kg
(approximately forty 325 mg [regular strength] or twenty-five 500 mg [extra strength]
tablets for an 80 kg adult) in an acute ingestion is generally required before significant
liver toxicity occurs; however, history alone may not be reliable. TOXICDOSE : >
200mg /kg in <12 yrs or 7.5 g single ingestion in adoloscent
If the serum acetaminophen concentration is on orabove the treatment line (that starts at 150
μg/mL at 4 hours anddecreases to 4.7 μg/mL at 24 hours), this indicates the need fortreatment
with NAC. If the serum acetaminophen concentrationis below the treatment line and the most
severe possible scenariohas been taken for the time of ingestion, then the patient requiresno
antidote. Use of the treatment line is a highly sensitive approachand may be used for patients
presenting after acute ingestions.
STAGE TIME AFTER CHARACTERISTICS
INGESTION

I 0.5–24 hr Anorexia, nausea, vomiting, malaise, pallor, diaphoresis

II 24–48 hr Resolution of earlier symptoms; right upper quadrant abdominal pain

and tenderness; elevated bilirubin, prothrombin time, hepatic
enzymes; oliguria

III 72–96 hr Peak liver function abnormalities; anorexia, nausea, vomiting, and
malaise may reappear

IV 4 days–2 wk Resolution of hepatic dysfunction or complete liver failure

Investigations –
 CBC
 Renal Function tests
 Serum Electrolytes
 Liver Function Tests
 PT-INR, aPTT
 ECG
 ABG
 CXR
Treatment –

Stabilization and Supportive Care

In addition to supportive care as needed, the mainstay of managementis the initiation NAC
therapy when indicated. Supportive care includes management ofco-ingestions, and the
nausea and vomiting, hepatic injury, andrenal dysfunction related to acetaminophen
poisoning. Treatmentof these problems is based on general treatment principles and is
not acetaminophen-dependent (see general approach guidelines).
Decontamination
Activated charcoal (AC) effectively binds acetaminophen in vitro,and some limited studies
have suggested that early administrationof AC (within 1 to 2 hours post-ingestion) may
decrease thenumber of patients that require antidotal therapy. However, manypatients have
co-ingestions that may decrease mental status, andpatients with severe acetaminophen
poisoning often developvomiting, thus increasing the risk for aspiration of AC. Therefore,
use of AC should have no bearing on the determination of theneed for NAC therapy. Given
the lack of demonstrated efficacyin terms of improved outcome, and the risk of adverse
outcomefrom aspiration of AC, we do not recommend the use of ACfor acetaminophen
overdose when NAC therapy is readily availablewithin 8 hours following an acute potentially
hepatotoxicingestion.
Enhanced Elimination
Hemodialysis is not routinely used for acetaminophen overdose,because there is a highly
effective antidote with good clinicaloutcomes when given within 8 hours of ingestion.
However,hemodialysis may be helpful when the absorbed acetaminophen
burden is sufficient to cause hepatotoxicity despite usual doses ofNAC. Initiation of
hemodialysisshould only be considered for patientspresenting following an acute massive
ingestion with
 Highly elevated serum acetaminophen concentration (>1000 mg/L) at
 4 hours post-ingestion
 Hepatorenal syndrome (Cr >3.5)
 Metabolic acidosis with pH <7.30
 Encephalopathy
 Elevated lactate (>3.5 mmol/L)
There is no definitive evidenceregarding the efficacy of hemodialysis in this setting, but
removalof excess acetaminophen may prevent hepatotoxicity by allowingthe NAC to
effectively deal with the reduced burden of toxin.
N-Acetylcysteine - When indicated, NAC should be administered as early as possible.Delay
of NAC more than 8 hours after ingestion increases the riskof hepatotoxicity.NAC can be
administered per os(by mouth; PO) or IV. Bothmethods are efficacious in most situations,
with advantages anddisadvantages for each. All formulations of NAC (PO or IV) arevery
effective when started within 8 hours of ingestion.Whenadministered early (<8 hours) the risk
of liver injury (ie, AST >1000 IU/L) inpatients treated with NAC within 8 hours is less than
4% and themortality rate approaches zero. IV NACdecreases the risk of hypotension, cerebral
edema, and death inpatients with acetaminophen-related hepatic failure.Oral NACshould only
be used if IV NAC is not available.Approximately 2% to 6% of patients treated with IV
NACdevelop significant anaphylactoid reactions.
NAC is safe and effective in pregnancy and effectively crosses the placenta. NAC is used
with the same protocolsas for the nonpregnant patient.
NAC administration protocol – Thestandard IV NAC protocol in adults is a loading dose of
150 mg/kg (Max 15gm) in 200 mL of dextrose 5% in water(D5W) infused over 60 minutes
followed by a first maintenancedose of 50 mg/kg (up to a maximum of 5 gm) in 500 mL
D5Winfused over 4 hours followed by a second maintenance dose of100 mg/kg (up to a
maximum of 10 gm) in 1000 mL D5W infusedover 16 hours (6.25 mg/kg/hour).
NAC therapyshould continue until acetaminophen is undetectable in theserum and signs of
liver injury have resolved(ie, no encephalopathy, normalization of the coagulationprofile,
resolution of metabolic acidosis) and the AST <1000 IU/L with a downward trend.
Disposition Criteria -
Asymptomatic patients who fit the criteria for treatment shouldbe treated with NAC, which
can be administered in a medicalinpatient unit or an emergency department observation unit.
Themotivation behind any ingestion needs to be evaluated, and psychiatricconsultation is
obtained when appropriate.
Patients showing evidence of severe hepatotoxicity and thoseat risk for fulminant hepatic
failure may need to be admitted to amonitored bed or an intensive care unit. These patients
requirefrequent neurologic checks, monitoring of vital signs, and repeatedlaboratory studies.
Pesticide Poisoning(29–33)

Pesticide Classes and Examples

Organophosphates Parathion, malathion
Carbamates Aldicarb, carbaryl
Chlorinated hydrocarbons Dichlorodiphenyltrichloroethane (DDT),
Lindane
Substituted phenols 2,4-dinitrophenol (DNP)
Bypyridyl pesticides Paraquat, diquat
Pyrethrins/pyrethroids Permethrin
Glyphosate N-(phosphonomethyl)glycine
Insect repellent N,N-Diethyl-meta-toluamide (DEET)
Organophosphorus Poisoning

Organophosphates are a class of insecticide pesticides that work by inhibiting cholinesterases,

including acetylcholinesterase and pseudocholinesterase. This is both the mechanism of their
efficacy as insecticides as well as their toxicity in humans. Inhibition of cholinesterases result
in accumulation of acetylcholine at multiple receptors within the autonomic nervous system,
the sympathetic and parasympathetic ganglionic nicotinic sites, postganglionic cholinergic
sympathetic and parasympathetic muscarinic sites, skeletal muscle nicotinic sites, and central
nervous system sites. Organophosphates are lipid soluble and are absorbed through
dermal, gastrointestinal, and respiratory routes. This can lead todeposition in fat tissues
allowing for possible toxicity from acuteand chronic, low-level exposures. Some
organophosphates haveactive metabolites that can result in delayed toxicity.
Clinical Features –
Organophosphate toxicity is represented by the ―SLUDGE‖ or―DUMBELS‖ syndrome
manifested by accumulation of acetylcholineat receptor sites. Muscarinic acetylcholine
accumulation leads to salivation, lacrimation,urinary incontinence, defecation, emesis,
bronchospasm,bronchorrhea, and bradycardia. Nicotinic acetylcholine accumulation
leads to tachycardia, tachydysrhythmias, and skeletal musclefasciculations.At the
neuromuscular junction, excess acetylcholine causeshyperstimulation of the muscles with
secondary paralysis, andwhen the diaphragm is affected, cholinesterase poisoning leads to
respiratory arrest. Sympathetic stimulation can lead to diaphoresis.A combination of
sympathetic stimulation, involvement of theN-methyl-d-aspartate (NMDA) receptor, and
enhanced acetylcholineconcentrations can induce seizures.Pulmonary edema can occur in
organophosphate poisoningand should not be confused with bronchorrhea or bronchospasm.
All these factors contribute to respiratory failure.A unique feature of organophosphate
insecticides is the processcalled aging, the irreversible conformational change that
occurswhen the organophosphate is bound to the cholinesterase enzymefor a prolonged time.
This causes the clinical effects to persist forperiods of days to weeks. The time to aging
varies by the specificproduct involved. Once an enzyme has aged, an oxime antidotecannot
be used to regenerate the cholinesterase.
Assess flexor neck strength regularly in conscious patients by asking them to lift their head
off the bed and hold it in that position while pressure is applied to their forehead. Any sign of
weakness is a sign that the patient is at risk of developing peripheral respiratory failure
(intermediate syndrome).
Intermediate Syndrome – An intermediate syndromemay occur 1 to 5 days after an
organophosphateexposure, reported in up to 40% of patients following ingestion.
Clinical features include paralysis of neck flexor muscles, muscles innervatedby the cranial
nerves, proximal limb muscles, and respiratorymuscles; respiratory support may be needed.
Symptoms or signs ofcholinergic excess are usually absent in this syndrome.
Electromyography mayassist in making the diagnosis. Aggressive, early antidote therapy
andsupportive measures may prevent or ameliorate the severity of this syndrome.Symptoms
usually resolve within 7 days.
Investigations -
 CBC  CXR
 Renal Function tests  Pseudocholinesterase - Normal
 Serum Electrolytes serum acetylcholinesterase level is

 ABG 8.0-20.0 u/l

 ECG
Treatment -
Treatment of organophosphate poisoning is directed toward fourgoals:
(1) decontamination
(2) supportive care with an emphasison respiratory stabilization
(3) reversal of acetylcholine excess,
(4) reversal of toxin binding at receptor sites on the cholinesterasemolecule.
The severity of the patient‘s signs and symptomsguides management.
 Supportive Care – Death in these cases is a result of airway and respiratory failure,
and therefore supportivecare should be directed primarily toward airway management
andinclude suctioning of secretions and vomitus, oxygenation, and,when necessary,
ventilatory support. Ensure that the two IV drips have been set up (one for fluid and
drugs, the other for atropine). Give 500–1000 ml (10–20 ml/kg) of normal saline over
10–20 min.
o Succinylcholine, 1.5 mg/kg, though commonly used as a paralytic drug for
emergency orotrachealintubation, is metabolized by cholinesterasesand may
have a prolonged duration of effect (4 to 6 hours) inthe setting of
organophosphate poisoning. If succinylcholineis used as a paralytic drug,
anticipate the need for prolongedsedation and ventilatory support.
o A nondepolarizing paralytic drug not metabolized by cholinesterases
(such as, rocuronium, 1 mg/kg) is preferable.
o Tachycardia and tachyarrhythmia generally resolves by treating the underlying
cholinergic excess and should not be treated symptomatically.
o Patients with agitation, seizures, and coma should be treated with adequate
doses of a benzodiazepine after the airway has beensecured.
 Decontamination - The first step in the management of patients with
organophosphate poisoning is putting on personal protective equipment. These
patients may still have the compound on them, and you must protect yourself.
Secondly, you must decontaminate the patient. This means removing all clothes
because it may be contaminated even after washing. The patient‘s skin needs to
be flushed with water. Activated charcoal can be given if the patient presents
within 1 hour of ingestion, but studies have not shown a benefit.
 Reversal of Ach Excess - The definitive treatment for organophosphate poisoning is
atropine, which competes with acetylcholine at the muscarinic receptors.The initial
dose for adults is 2 to 5 mg IV or 0.05 mg/kg IV for children until reaching the adult
dose. If the patient doesn‘t respond, double the dose every 3 to 5 minutes until
respiratory secretions have cleared and there is no bronchoconstriction. In patients
with severe poisoning, it may take hundreds of milligrams of atropine over several
days before the patient improves.
o Target Endpoints of Atropine –
 Clear chest on auscultation with no wheeze
 Heart rate> 80 beats/min
 Pupil no longer pin point
 Dry axilla
 Systolic blood pressure > 80 mm of Hg
Tachycardia is not a contraindication to atropine since it can be caused by
many factors. The pupils will commonly dilate; however, this sign is not a
useful endpoint for initial atropine treatment because a delay exists before
maximum effect.
Atropine maintenance: - Target end point once achieved is to be maintained by
atropine infusion. Infusion of atropine reduces the fluctuation in atropine
concentration associated with repeated bolus doses. The rate of infusion is set at 10 -
20 % of the total atropine required to load the patient every hour. The patient must be
closely monitored and vitals documented to watch for further cholinergic crises or
atropine toxicity.
 Duration of maintenance atropine therapy: - This depends on the severity and
response to therapy. Usually it is maintained for 24- 48 hrs or longer in severe cases,
and gradually withdrawn over 3-5 days. Frequent observation is required to detect
early signs of intermediate syndrome.

 Reactivation of enzyme - Pralidoxime (2-PAM) also should be given to affect the

nicotinic receptors since atropine only works on muscarinic receptors. Atropine must
be given beforePAM to avoid worsening of muscarinic-mediated symptoms. A bolus
of at least 30 mg/kg in adults or 20 to 50 mg/kg for children should be given over 30
minutes. Rapid administration can cause cardiac arrest. After the bolus, a continuous
infusion of at least 8 mg/kg/hr for adults and 10 to 20 mg/kg/hr for children should be
started and may be needed for several days.
 Ventilator Settings - This is the most useful advance in the management of OP
poisoning and makes all the difference on outcome.Consider intubation and ventilate
patients if patient has respiratory failure and poor neck power, tidal volume is below 5
 mL/kg or if they have apnoeic spells, or PaO2 is less than 8 kPa (60 mm Hg) on
FIO2 of more than 60%. Tidal volume should be checked every 4 h in such patients.
Succinylcholine is to be avoided and Non-depolarising neuromuscular blocking
agents require higher doses to show effect.
 Others - Treat agitation by reviewing the dose of atropine being given and provide
adequate sedation with benzodiazepines. Physical restraint of agitated patients in
warm conditions risks severe hyperthermia, which is exacerbated greatly by atropine
because it inhibits normal thermoregulatory responses including sweating. Adequate
sedation is therefore important. Monitor frequently for recurring cholinergic crises
due to release of fat soluble OP from fat stores. Such crises can occur for several days
to weeks after ingestion of some OP. Patients with recurring cholinergic features will
need retreatment with atropine and oxime.
Disposition -
Most patients who present to the ED after significant organophosphateexposure should be
admitted to a monitored setting. Theeffects of organophosphate intoxication can be
prolonged. Patients who present with significant symptoms (acuterespiratory compromise
associated with depressed cholinesteraselevels) require admission and close monitoring,
usually in anintensive care unit (ICU). Patients may have rebound toxicityseveral days after
apparently satisfactory response to initial treatment.This may occur for many reasons,
including persistentrelease of organophosphates from lipid stores.
Poisoning withfenthion is of particular concern, because initial symptoms couldbe mild and
progress to life-threatening intoxication over time.
Patients with acts of self-harm or suicidal intent requirepsychiatric consultation.
Intermediate Syndromecan present with delayedparalysis, and occurs 24 to 96 hours after the
resolution of the cholinergic crisis. Theprecise cause of IMS is not well documented.
Delayedperipheral neuropathy may occur 7 to 21 days after acute
organophosphateintoxication. Therefore, close patient follow-up isimportant even after
stabilization.
Rodenticide Poisoning – Rat Poison ingestion(29,34–40)

These are compounds which kill rats, mice, moles, and other rodents.
Examples are anticoagulants, thallium, vacor, phosphorus,zinc and aluminium phosphide,
alpha-naphthyl-thiourea,cholecalciferol, arsenic, barium carbonate, bromethalin.
Aluminum Phosphide/Zinc Phosphide Poisoning –
Prior to 1980, aluminium phosphide poisoning was virtuallyunreported in India. Today it is
the leading cause of suicidal(and sometimes accidental) death in northern Indian states and
there areominous indications of a gradual rise in the number of casesbeing reported.
Aluminium phosphide is marketed in India under varioustrade names (Alphos, Bidphos,
Celphos, Chemfume, Delicia,Fumigran, Phosphotek, Phosphume, Phostoxin, Quickphos,
Synfume, etc.).It is generally available as greyish green tablets of 3 gramseach, mixed with
urea and ammonium carbonate. These tablets are sold in sealed, airtight containers of tens
andtwenties. Each tablet liberates 1 gram of phosphine.
When exposed to air and moisture, aluminium phosphide liberatesphosphine which causes
multi-organ damage.
AlP + 3H2O→Al(OH)3 + PH3
Clinical Features
1. Common presenting symptoms include metallic taste,vomiting, garlicky (or fishy) odour of
breath, intense thirst,burning epigastric pain, and diarrhoea.
2. In severe cases, there are cardiovascular manifestationssuch as:
 Hypotension
 Tachy/bradycardia
 ECG abnormalities:
o sinus tachycardia, sinus o T wave inversion in V5-
arrhythmia 6,sinus arrest, chaotic atrial
o ST segment depression in pacemaker
lead II, III, and AVF, o Complete heartblock,
o STelevation bundle branch block and
o Atrial fibrillation VPCs/VT.
 Massive focal myocardial injury with elevated serumlevels of cardiac enzymes.
3. Convulsions have been reported in some cases. Comasupervenes in later stages.
4. Hepatic damage, renal failure, and metabolic acidosis arepossible.
5. Respiratory distress is invariably present with cyanosis, andcold, clammy skin.
Diagnosis and Investigations –
 Garlicky odour in the breath.
 Urinalysis may reveal occult blood, bilirubin, glucose, and albumin.
  Liver function tests are often abnormal.
 Blood urea and serum creatinine are usually higher than normal.
 Hypo/hypermagnesaemia; hypo/hyperphosphataemia.
 ECG changes (mentioned under Clinical Features)
Treatment
 Emesis is not to be induced. To reduce the absorption of phosphine gastric lavage
with potassium permanganate (1:10,000) is done. Potassium permanganate (1:10000)
is used as it oxidizes PH3 to form non-toxic phosphate. This is followed by slurry of
activated charcoal (approximately 100 g) given through a nasogastric tube.
 Correction of plasma glucose level can help the patient to get better.
 The most important factor for success is resuscitation of shock and institution of
supportive measures as soon as the patient‘s arrival. IV line should be established and
2–3 liters of normal saline should be given within the first 8–12 h guided by central
venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP). The aim is
to keep the CVP at around 12–14 cm of water. Hydrocortisone 200–400 mg every 4–
6 h is given intravenously to combat shock, check capillary leakage in lungs (ARDS)
and to potentiate the responsiveness of the body to catecholamines.
 Management of respiratory distress with 100% humidified oxygen, intubation.
 Phosphine excretion can be increased by maintaining adequate hydration and renal
perfusion with intravenous fluids and diuretics like furosemide can be given if systolic
blood pressure is >90 mm Hg to enhance excretion as the main route of elimination of
phosphine is renal. All types of ventricular arrhythmias are seen in these patients and
the management is the same as for arrhythmias in other situations.
 Bicarbonate level less than 15 mEq/L requires sodabicarb in a dose of 50–100 mEq
intravenously every 8 hour till the bicarbonate level rises to 18–20 mEq/L. Patients
may require up to 300–500 ml of sodium bicarbonate [59]. Dialysis may be required
for severe acidosis and acute renal failure [3].
 Hypo-magnesemia is a common outcome of acute poisoning of phosphine gas
exposure and intracellular magnesium plays an important role as a co-factor in the
synthesis and activity of glutathione and other antioxidants. Intravenous magnesium
administration showed significant improvement in indicators of oxidative stress and a
lower incidence of mortality (20%) in comparison to control subjects (44% mortality).
 Magnesium sulfate 1 gram can be given IV to begin with, followed each hour by the
same dose for 3 consecutive hours, and then 1 gram every 6 hours for 5 days.
 Control of convulsions with anticonvulsants (80enzodiazepines, barbiturates, etc.)
Corrosive Ingestion
I )Acids and Alkali Ingestions
Caustics are substances that cause both functional and histologic damage on contact with
body surfaces.Many household and industrialchemicals have caustic potential. Caustics are
broadly classified as alkalis(pH >7) or acids (pH <7).
Factors that influence the extent of injury from a causticexposure include type of agent,
concentration of solution, volume,viscosity, duration of contact, pH, and presence or absence
of foodin the stomach.
Acidic compounds desiccate epithelial cells and cause coagulationnecrosis. An eschar is
formed that limits further penetration. Acids tend to have a strong odor and cause
immediatepain on contact, hence the quantity ingested is usually limited.
Alkaline contact, in contrast to acids, causes liquefaction necrosis,fat saponification, and
protein disruption, allowing furtherpenetration of the alkaline substance into the tissue. The
depth ofthe necrosis depends on the concentration of the agent. Alkalis are colorless and
odorlessand do not cause immediate pain on contact so amount consumed is usually more.
Clinical Features -
 Airway edema and esophageal/gastric perforations are the most emergent issues.
Laryngeal edema begins in minutes and occurs over several hours.
 Systemic toxicity, hypovolemic shock, and hemodynamic instability with hypotension,
tachycardia, fever, and acidosis are ominous signs.
 Small ingestions of potent substances can be as serious as larger ingestions. Patients with
acid or alkali ingestions present with similar initial constellation of signs and symptoms.
 Oral pain, abdominal pain, vomiting, and drooling are common. Patients can have
wheezing, coughing, respiratory distress, hoarseness, odynophagia, dysphagia, stridor.
 Chest pain is common.
 Visible burns to the face, lips, and oral cavity may be seen. Skin burns can occur from
spillage or secondary contamination after vomiting.
 Peritoneal signs suggest hollow viscus perforation.
 Tracheal necrosis is one of the most frequent causes of death after caustic ingestion.
 Oropharyngeal burns are not predictive of distal injury, but drooling, odynophagia,
vomiting, and stridor, in combination, are highly predictive of significant lesions.
 Dysphagia usually subsides in 3 to 4 days. Patients with significant esophageal burns may
develop esophageal stricture. Symptoms include dysphagia and food
impactions.Strictures that are symptomatic early are generally more severe.
 Patients with significant esophageal injury have a thousandfold increase in esophageal
carcinoma, which develops 40 to 50 years after the caustic ingestion. Nearly 3%
ofesophageal cancer patients have a history of caustic ingestion.
Investigations –
CBC Chest X ray – Erect
RFTs, Serum Electrolyes CT thoracoabdominal – If Oesophageal
ECG injury is suspected.
ABG – Can show Anion gap acidosis
Treatment –
 Airway maintenance -
o The first priority is airway maintenance. Patients with respiratory distress may
have significant oral, pharyngeal, and/or laryngotracheal injuries that require
emergent airway management. If emergency airway management precedes patient
decontamination, prevent exposure to the ED staff. Caustic airway injuries are
difficult airways. Ideally, patientswith potential airway injuries should have
fiberoptic evaluation before intubation, but this may not always be possible. Blind
nasotracheal intubation is contraindicated due to the potential for exacerbating
airway injuries. Oral intubation with direct visualization is the first choice for
definitive airway management
 Decontamination, neutralization, and dilution -
o The ED staff should take precautions to prevent ongoing injury to the patient and
staff from continued caustic exposure. ED staff involved should wear protective
gowns, gloves, and masks. Standard decontamination, with removal of soiled or
soaked clothing and copious irrigation with towels and soap, is adequate in most
cases. Vomiting may re-expose patient and staff to the caustic agent.
o Gastric decontamination with activated charcoal is contraindicated if a
caustic is the only ingestion. Charcoal does not adhere well to most caustics and
will impede visualization during endoscopy.Emetics are contraindicated, because
vomiting will result in repeat exposure of the airway and GI mucosa to the caustic
agent and could precipitate perforation.
o Do not insert NG tubes until after endoscopy.
 Fluid resuscitation
o Establish large-bore IV access and resuscitate with crystalloids.
o Central venous access may be required for monitoring of resuscitation.
 Systemic steroids and prophylactic antibiotics
o There is currently no evidence of consistent benefit from systemicsteroids or
prophylactic antibiotics.
Disposition - Admit all patients with symptomatic caustic ingestions.
II ) Corrosives - Phenol and Formaldehyde
Ingestion of phenol or formaldehyde can also cause severe causticinjury to the GI tract. Both
phenol and formaldehyde are generalprotoplasmic poisons and can cause protein denaturation
andcoagulation necrosis.
Systemic symptoms, include dysrhythmias,hypotension, seizures, and coma. Acidosis may be
prominent after formaldehydeingestion because of its metabolism to formic acid. Phenol is
wellabsorbed through the skin, and dermal exposure may result inburns and systemic toxicity.
Hydrocarbon aspiration causes chemical pneumonitis by direct toxicityto the pulmonary
parenchyma and alteration of surfactant function.Destruction of alveolar and capillary
membranes results in increasedvascular permeability and edema. The clinical manifestations
of pulmonaryaspiration are usually apparent soon after exposure from irritationof the oral
mucosa and tracheobronchial tree. Symptoms include coughing,choking, gasping, dyspnea,
and burning of the mouth. Patients withthese symptoms should be assumed to have
aspirated.Signs include tachypnea, grunting respirations, wheezing, or retractionsdepending
on the severity of aspiration. An odor of the hydrocarbonmay be noted on the patient‘s
breath. Hyperthermia of ≥39°C(≥102.2°F) is likely and may occur initially or 6 to 8 hours
after exposure.The fever is usually an inflammatory response due to pneumonitis.Necrotizing
pneumonitis and hemorrhagic pulmonary edema maydevelop within minutes to hours in
patients with severe aspiration. Inmost fatalities, these complications occur rapidly.
X-ray Changes may be seen as early as 30 minutes afteraspiration, but the initial radiograph
in a symptomatic patient may be deceptively clear. Conversely, an asymptomatic patient can
still have abnormal chest radiographic findings later during the clinical course. The most
worrisome acute complication found in solvent abusers is ―sudden sniffing death syndrome‖
and occurs within minutes of exposure. Themechanism of toxicity is believed to be
catecholamine sensitization ofthe heart by hydrocarbons resulting in dysrhythmias
Treatment -
o Airway and breathing - Secure airway and provide supplemental oxygen.
o Antidotes: Administer oxygen for carboxyhemoglobinemia and methylene blue
for methemoglobinemia.
o Administer inhaled β2-agonists.
o Ventilatory support: Provide positive end-expiratory pressure or CPAP as needed
to achieve adequate oxygenation.
 Cardiac Circulation:
o Administer IV crystalloid fluid for volume resuscitation of hypotensive patients.
o Do not use catecholamines in cases of halogenated hydrocarbon exposure.
o Consider propranolol, esmolol, or lidocaine for ventricular dysrhythmias induced
by halogenated hydrocarbon exposure.
 Decontamination Dermal:
 o Remove hydrocarbon-soaked clothes, decontaminate skin with soap and water,
and decontaminate eyes with saline irrigation.
o GI: Not indicated. See discussion below.
 Other Laboratory tests:
o Order CBC, basic metabolic panel, liver function tests (serum transaminase,
bilirubin, albumin levels), prothrombin time, partial thromboplastin time,
carboxyhemoglobin level, methemoglobin level, and/or radiologic studies as
indicated.
 Correct electrolyte abnormalities.
 Administer blood products as needed.

Snake Bite(7,29,41–44) add ministry guideline cite

There are more than 2000 species of snakes in the world and about 300 species are
found in India out of which 52 are venomous. India is estimated to have the highest snakebite
mortality in the world. World Health Organization (WHO) estimates place the number of
bites to be 83,000 per annum with 11,000 deaths. The venomous snakes found in India
belong to three families Elapidae, Viperidae and hydrophidae (Sea Snakes). Themost
common Indian elapids are Najanaja(Indian Cobra) and Bungarus caeruleus(Indian Krait),
Daboia russalie(Russells‘ Viper) and Echiscarinatus(Saw scaled viper).
Kraits are active during night hours,often biting a person sleeping on floor bed. Maximum
Viper and Cobra bites occurduring the day or early darkness, while watering the plantation or
walking bare footin grown grass or soybean crops.
Clinical presentation of snakebite victim depends upon
 Species of snake
 Amount of venom injected
 Site of bite, area covered or uncovered
 Dry or incomplete bite, multiple bites,
 Weight of the victim
 Time elapsed between the bite and administration of ASV.
 Venom concentration and constitution depends on environmental conditions as well as
snake‘s maturity and darkness of colour of snake. \
Patients present in the four clinical syndromes or in combination i.e. progressive weakness
(neuroparalytic/neurotoxic), bleeding (vasculotoxic/haemotoxic), myotoxic and painful
progressive swelling.

Clinical Features and Presentation –

 Asymptomatic (i.e., non Venom related symptoms)
Patients many a times present with nonspecific symptoms related to anxiety.Common
symptoms in these patients are:– Palpitations, sweating, tachycardia, tachypnoea,
elevatedblood pressure, cold extremities and paraesthesia. These patients may havedilated
pupils suggestive of sympathetic over activity.Redness, increased temperature, persistent
bleeding and tenderness may be present locally.However, local swelling can be present in
these patients due to tight ligature
 Dry Bite
Bites by nonvenomous snakes are common and bites by venomous speciesare not always
accompanied by the injection of venom (dry bites).The percentage of dry bites ranges from
10–80% for various poisonoussnakes.Some people who are bitten by snakes (or suspect or
imagine that they havebeen bitten) or have doubts regarding bite may develop quite striking
symptoms and signs, even when no venom has been injected due to fear of a venomous
bite.Even in case of dry bite, symptoms due to anxiety and sympathetic overactivity(as
above) may be present. As symptoms associated with panic orstress sometimes mimic early
envenomation, clinicians may havedifficulties in determining if envenoming occurred or not.
 Neuroparalytic (Progressive weakness; Elapid envenomation)
o Neuroparalytic snakebite patients present with typical symptoms within 30min– 6hrs
in case of Cobra bite and 6 – 24 hours for Krait bite; however, ptosis in Krait bite
have been recorded as late as 36 hours after hospitalization.
o These symptoms can be remembered as 5 Ds and 2 Ps.
 5 Ds – dyspnea, dysphonia, dysarthria, diplopia, dysphagia
 2Ps – ptosis, paralysis
o In chronological order of appearance of symptoms – furrowing of forehead,
Ptosis >Diplopia >Dysarthria>Dysphonia>Dyspnoea>Dysphagia
o All these symptoms are related to 3rd, 4th, 6th and lower cranial nerve paralysis.
Finally, paralysis of intercostal and skeletalmuscles occurs in descending manner.
Reduced/absent tendon reflexes & head lag are signs of impending respiratory failure
o Additional features like stridor, ataxia may also be seen.
o Associated hypertension and tachycardia may be present due to hypoxia.
o To identify impending respiratory failure use bedside lung function tests viz.
 Single breath count – number of digits counted in one exhalation - >30 normal
 Breath holding time – breath held in inspiration – normal > 45 sec
 Ability to complete one sentence in one breath.
 Cry in a child whether loud or husky can help in identifying failure.
o Patients presenting with these symptoms require Atropine Neostigmine injection.
 Vasculotoxic (haemotoxic) - General signs and symptoms of Viperine envenomation)
 Local manifestations –Russel‘s viper > Saw scaled viper > Pit viper bite.
 Local manifestations are in form of:
o Local swelling, bleeding, blistering, and necrosis.
o Pain at bite site and severe swelling leading to compartment syndrome.
o Pain on passive movement.
o Absence of peripheral pulses and hypoesthesia.
o Tender enlargement of local draining lymph node.
  Systemic manifestations –
 Visible systemic bleeding e.g. gingival bleeding, epistaxis, ecchymoses, hematemesis,
hemoptysis, bleeding per rectum, subconjunctival hemorrhages, bleeding from the bite
site, bleeding from pre-existing conditions (bleeding from freshly healed wounds).
 Bleeding or ecchymosis at the injection site is a common finding in Viper bites.
 The skin and mucosacan show petechiae, purpura, ecchymosesand gangrene.
 Swelling and local pain.
 Acute abdominal tenderness may suggest GI or retroperitoneal bleeding.
 Lateralizing neurological symptoms may be indicative of IC bleeding.
 Consumption coagulopathy detectable by WBCT, develops as early as within 30 minutes
from time of bite but may be delayed.
 Life threatening complications are due to renal involvement. Patient presents with
hematuria, hemoglobinuria, myoglobinuria followed by oliguria and anuria with acute
kidney injury (AKI).
o Bilateral renal angle tenderness.
o Passage of discolored (reddish or dark brown urine or declining urine output)
o Acute Kidney Injury e.g. declining or no urine output, deteriorating renal signs
such as rising serum creatinine, urea or potassium.
o Hypotension due to hypovolaemia or direct cardiotoxicity aggravates AKI.
o Parotid swelling, conjunctiva oedema, sub-conjunctival haemorrhage, renal
failure, acute respiratory distress syndrome and refractoryshock.
o Long term sequelae e.g. pituitary insufficiency with Russell‘s viper
 Painful Progressive Swelling (PPS)
o Due to local venom toxicity and is prominent in Russel‘s and Saw scaled viper
and Cobra bites.
o Local necrosis of limb which often has a rancid smell.
o Limb is swollen and the skin is taut and shiny. Blistering with reddish black fluid
at and around the bite site. Skip lesions around main lesion are also seen.
o Ecchymoses due to venom action destroying blood vessel wall.
o Compartment syndrome will present invariably.
o Regional tender enlarged lymphadenopathy.
 Myotoxic - This presentation is common in Sea snakebite. Patient presents with:
o Muscle aches, muscle swelling, involuntary contractions of muscles.
o Passage of dark brown urine.
o Compartment syndrome, cardiac arrhythmias, AKI due to myoglobinuria
 Occult snakebite - Krait bite victims often present in the early morning with paralysis with
no local signs. Krait has nocturnal habitat and has fine slender teeth. Hence bite marks
 usually cannot be identified even on close examination. Typical presenting history is that the
patient was healthy at night, in the morning gets up with severe epigastric/umbilical pain with
vomiting followed by typical neuroparalytic symptoms. There is no history of snakebite.
 Unexplained respiratory distress in children in the presence of ptosis or sudden onset of acute
flaccid paralysis in a child (locked-in syndrome) is highly suspicious of Krait bite.
Investigations - Lab tests are of little value in the diagnosis of snake envenomation, but can
be useful for prognosticating and for making decisions about specific interventions.
The 20-min whole blood clotting test (20 WBCT): The 20 WBCT is a simple bedside test
of coagulopathy to diagnose viper envenomation and rule out elapid bite. It requires a new
clean, dry test tube made up of simple glass that has not been washed with any detergent. A
few milliliters of fresh venous blood is drawn and left undisturbed in the test tube for 20 min;
the tube is then tilted gently. If the blood is still liquid after 20 min, it is evidence of
coagulopathy and confirms that the patient has been bitten by a viper. Cobras or kraits do not
cause antihemostatic symptoms.
i. CBC vii. Electrocardiogram (ECG):
ii. Serum creatinine Nonspecific ECG changes such as
iii. Serum amylase and CPK: Elevated bradycardia and atrioventricular
levels suggest muscle damage. block with ST-T changes may be
iv. PT, aPTT seen.
v. ABG, Serume electrolytes viii. The first blood drawn from the
vi. Urine examination: Can patient should be typed and cross-
showhematuria, proteinuria, matched, as the effects of both
hemoglobinuria, myoglobinuria. venom and antivenom can interfere
with later cross-matching.
Assessment of severity of envenomation
No envenomation Absence of local or systemic reactions; fang marks (+/−)

Mild envenomation Fang marks (+), moderate pain, minimal local edema (0–15 ce),
erythema (+), ecchymosis (+/−), no systemic reactions

Moderate envenomation Fang marks (+), severe pain, moderate local edema (15–30 cm),
erythema and ecchymosis (+), systemic weakness, sweating,
syncope, nausea, vomiting, anemia, or thrombocytopenia

Severe envenomation Fang marks (+), severe pain, severe local edema (>30 cm), erythema
and ecchymosis (+), hypotension, paresthesia, coma, pulmonary
edema, respiratory failure
 Treatment –

# ASV indicated in rapidly developing swelling only. Purely localized swelling with or without bitemarks
is not an indication of ASV.
** For reaction to antisnake venom (ASV) Dose of Adrenaline 0.5 mg IM (in children 0.01mg/kg)
¥ Specific ASV for sea snake and Pit viper bite is not available in India. However, available ASVmay
have some advantage by cross reaction.
*** Atropine 0.6 mg followed by neostigmine (1.5mg) to be given IV stat (In children Inj. Atropine0.05
mg/kg followed by Inj. Neostigmine 0.04 mg/kg IV.) Repeat neostigmine dose 0.5 mg (inchildren
0.01mg/kg) with atropine every 30 minutes for 5 doses. Thereafter, taper dose at 1hour, 2 hour, 6 hours
and 12 hours. Positive response is measured as 50% or more recovery ofthe ptosis in one hour. If no
response after 3rd dose. Stop AN injection.
Treatment is divided into the following headings –
1) Stabilisation of ABCs and Supportive care
2) Anti Snake Venom
3) Atropine-Neostigmine Treatment
4) Antibiotics
5) Coagulopathy Management
6) Surgical measures
1) Supportive Care –
o Manage the ABCs of the patient
o Provide Oxygen if necessary and handle respiratory arrest or life threatening bleed
o Assisted ventilation. The duration of mechanical ventilation in snakebite victims
is usually short since neuroparalysis reverses quickly with prompt administration
of ASV. Manual ventilation (self ventilating anaesthetic bag) has been effective.
o If the patient has intravascular volume depletion,proceed as follows:
o Establish intravenous access.
o Fluid challenge: 2l of isotonic saline over one hour
o Observe the patient closely to watch for pulmonary oedema.
2) Antisnake Venom –
o Anti-snake venom (ASV) is the mainstay of treatment. In India, polyvalent ASV,
i.e. effective against all the four common species; Russell‘s viper, common cobra,
common Krait and saw-scaled viper and no monovalent ASVs are available.
There are species such as the humpnosed pit viper where ASV is ineffective.
o Indications for anti-snake venom
System Clinical features

Haematological Spontaneous systemic bleeding

and General Whole blood clotting time >20 min, Thrombocytopenia<100,000/mm3

Shock

Arrhythmia, Abnormal electrocardiogram

Neurological Ptosis and paralysis

Renal Acute renal failure

Generalized rhabdomyolysis and muscular pains

Hyperkalemia

Local Local swelling involving more than half of the bitten limb

Rapid extension of swelling – Crossing at least one joint

Development of an enlarged lymph node draining the bitten limb

If ASV is indicated i.e. signs and symptoms of envenomation with or withoutevidence of
laboratory tests, administer full dose. There are no absolute contraindications to ASV.
Dose of ASV – ASV shouldbe administered by intravenous infusion (antivenom diluted in 5–
10 ml per kilogram body weight of normal saline or D5 W and infused over 1 h).
Dose for neuroparalytic snakebite – ASV 10 vials stat as infusion over30 mins followed by
2nd dose of 10 vials after 1 hour if no improvement within 1sthour.
Dose of ASV for vasculotoxic snakebite - Two regimens low dose infusiontherapy and high
dose intermittent bolus therapy can be used. Low dose infusiontherapy is as effective as high
dose intermittent bolus therapy and also saves scarceASV doses (Expert Consensus).
– Low Dose infusion therapy – 10 vials for Russel‘s viper or 6 vials for Saw scaled
viper as stat as infusion over 30 minutes followed by 2 vials every 6 hours asinfusion
in 100 ml of NS till clotting time normalizes or for 3 dayswhichever is earlier.
– High dose intermittent bolus therapy - 10 vials of polyvalent ASV stat over 30mins
as infusion, followed by 6 vials 6 hourly as bolus therapy till clottingtime normalizes
and/or local swelling subsides.
No ASV isto be given for Sea snakebite or pit viper bite as available ASV does not
containantibodies against them. No change in dose for Paediatric or in pregnant patients.
ASV reaction - Approximately 20% patients treated with ASV develop reactions.
 Early anaphylactic reactions - Occurs within 10–180 min of start of therapy and is
characterized by itching, urticaria, cough, nausea and vomiting, abdominal pain,
diarrhea, tachycardia, and fever. Patients may develop life-threatening anaphylaxis.
 Pyrogenic reactions usually develop 1–2 h after treatment. Symptoms include chills
and rigors, fever, and hypotension. These reactions are caused by contamination of
the ASV with pyrogens during the manufacturing process.
 Late (serum sickness–type) reactions develop 1–12 (mean 7) days after treatment.
Clinical features include fever, nausea, vomiting, diarrhea, itching, recurrent urticaria,
arthralgia, myalgia, lymphadenopathy, nephritis and, rarely, encephalopathy.
Treatment of ASV reaction
When the patient shows signs of a reaction, ASV administration must be temporarily
stopped and adrenaline (1 in 1000) given intramuscularly in an initial dose of 0.5 mg in adults
or 0.01 mg/kg body weight in children. The dose can be repeated every 5–10 min if needed.
An anti-H1 antihistamine such as chlorpheniramine maleate (adult dose 10 mg, children 0.2
mg/kg) should be given intravenously. Start oxygen and iv fluids to flush the line. It may be
followed by intravenous hydrocortisone (adult dose 100 mg, children 2 mg/kg).Role of
Hydrocortisone in managing ASV reaction is not proved.Late reactions usually respond to
a 5-day course of oral antihistamine. Patients who fail to respond should be given a 5-day
course of prednisolone (5 mg q6h in adults and 0.7 mg/kg/day in divided doses in children).
Late Presentationsof Snake Bite- Sometimes victims arrive late after the bite, often after
several days, usually withacute kidney injury. Determine current venom activity such as
bleeding in case ofviperine envenomation. Perform 20WBCT and determine if any
coagulopathy ispresent then administer ASV. If no coagulopathy is evident, treat kidney
injury, ifany.
 In patients with neuroparalytic envenomation, continue respiratory support until
recovery
 Give 10 vials of ASV on arrival and if no improvement within one hour repeat
 10 vials of ASV (No more than 20 vials of ASV).
 No further ASV and Atropine Neostigmine (AN) infusion is required ONLY to
reverse the ptosis if pharyngeal muscle palsy has resolved.
Monitoring of patients on ASV
 All patients should be watched carefully every 5 min for first 30 min, then at
 15 min for 2 hours for manifestation of a reaction. At the earliest sign of an
adverse reaction suspend temporarily.
3) Atropine and Neostigmine – Indicated in neuroparalytic snake bite.
o Atropine 0.6 mg followed by neostigmine (1.5mg) to be given IV stat and repeat
dose of neostigmine 0.5 mg with atropine every 30 minutes for 5 doses (In
children, Inj. Atropine 0.05 mg/kg followed by Inj. Neostigmine 0.04 mg/kg ivand
repeat dose 0.01 mg/kg every 30 minutes for 5 doses). A fixed dose combination
of Neostigmine and glycopyrolate IV can also be used.
o Thereafter to be given as tapering dose at 1 hour, 2 hour, 6 hours and 12 hour.
o Majority of patients improve within first 5 doses. Observe the patient closely
observed for 1 hour to determine if the neostigmine is effective. After 30mins, any
improvement should be visible by an improvement in ptosis.
o Positive response to ―AN‖ trial is measured as >50% recovery ofptosis in 1 hour.
o Stop Atropine neostigmine (AN) dosage schedule if:
• Patient has complete recovery from neuroparalysis. Rarely patient can have
recurrence, carefully watch patients for recurrence.
• Patient shows side effects in the form of fasciculations or bradycardia.
• If there is no improvement after 3 doses.
o Improvement by atropine neostigmine indicates Cobra bite.
o Give one dose of ―AN‖ injection before transferring or referring patient. Rapid
deterioration of Cobra bite neurotoxic syndrome may kill the patient on the way.
 Treatment Algorithm (For Bangalore Baptist Hospital Setup)

Important Points – Administer ASV 10 vials in

o There is no Contraindication for ASV 5%D over 1 hour
o Dose is the same for Paediatric patients.
o Treat reactions to ASV withAdrenaline(1 in 1000) im in a dose of
0.5 mg in adults or 0.01 mg/kg body weight in children. The dose
Consider Atropine-
can be repeated every 5–10 min if needed. Add an anti-H1
Neostigmine in Neurotoxicity
antihistamine such as chlorpheniramine maleate (adult dose 10
patients
mg, children 0.2 mg/kg)iv.
o Atropine 0.6 mg followed by neostigmine (1.5mg) IV stat and
repeat dose of neostigmine 0.5 mg with atropine every 30 minutes
for 5 doses. Administer Inj TT and
o WBCT to be repeated every half an hour regardless of whether it clots or
not in the ER.
Watch for Reactions to ASV
Clinical Features of
Neurotoxic/Vasculotoxic
Manage Vitals and with indication for ASV;
secure ABCs and triage Consider antibiotics
WBCT > 20mins (Amoxiclav/Cephalosporin)
patient to Priority I
if local reaction is severe
and perform dressing
Attempt to Identify the Investigations - WBCT
Snake and Spectrum of CBC, RFTs, S/E
Patient brought with PT-INR, aPTT, BT, CT Follow up blleding
suspected snake bite toxicity and features of parameters and treat
envenomation ECG, ABG, CXR
coagulopathy with
Urine Routine FFPs/Blood transfusions

WBCT - Draw blood in a

plain glass tube and check Admit the patient under
for coagulation in 20mins Medicine in HDU/ICU
based on vital parameters

No clinical features of Admit the patient in

envenomation or HDU/Ward for repeated
indication for ASV and bleeding parameters and to
WBCT < 20 mins watch for deterioration
4) Antibiotics - Give prophylactic broad-spectrum antimicrobial treatment for cellulitis after the
first 10 vials of ASV.
o Inj. Amoxiciilin+ clavulanic acid 1.2 g IV thrice daily for first 7 days
o In children, the dose is 100 mg/Kg/day in three divided doses intravenously
o Inj. Metronidazole 400 mg IV infusion thrice daily for 7 days;
o In children-30 mg/kg/day in 3-4 divided doses.
o Alternatively Inj Ceftriaxone 1 g IV twice daily (in children the dose is 100mg/kg/day in
two divided doses)for 7 days
o Both Amoxiciilin+ clavulanic acid and Ceftriaxone are mainly excreted through Kidney.
Therefore, in case of acute kidney injury in Viper bites dose of both these antibiotics
should be reduced and adjusted according to renal function.
5) Coagulopathy Management -
In case of prolonged CT, PT, aPTT administer freshfrozen plasma (FFP) infusion. Associated
low platelets indicates consumptivecoagulopathy and disseminated intravascular coagulopathy
(DIC). To confirmfibrinogen level FDP should be estimated.
Low fibrinogen and high FDP willrequire fibrinogen/FFP supplementation.
Bleeding leads to anaemia, PCV of at least 30% must be maintained, therefore, measure serial
PCV every 4 – 6 hdepending upon bleeding severity of patients. If PCV is lower than
30%bloodtransfusion/PCV transfusion needs to be arranged.
Avoid intramuscular injections.
The aim should be a return of coagulation function, asdefined by an INR of < 2.0, at 6 h after
ASV administration was commenced.
Heparin is ineffective against venom-induced thrombosis and may cause bleeding on its own
account. It should never be used in cases of snakebite. Antifibrinolytic agents are not effective
and should not be used in victims of snakebite.
6) Surgical Measures needed in Snake Bite -
Clean the bitten site with povidone-iodine solution, but do not apply anydressings. Leave blisters
alone. Allow them to break spontaneously and heal. If there islocal necrosis, excise and apply
saline dressings. Surgical decompression maybe necessary in some cases.
Administer booster dose of Tetanus toxoid injection.
Compartment syndrome is diagnosed with 5 ‗P‘ –
• Pain (severe) • Pulselessness
• Pallor • Paralysis or weakness of
• Paraesthesia compartment muscle.
Surgical consult is needed when compartment syndrome is suspected or patient has necrosis of the
limb. Early treatment with ASV remains the best way of preventingirreversible muscle
damage.
 Scorpion Sting(34,45)
The commonest species seen in India is Mesobuthustamulus(red scorpion) and Palamnaeus
species.As a general rule, scorpions with thick and powerful clawsare less toxic, while those with
slender claws are more toxic.Scorpions sting; they do not bite.
Mode of Action of venom -
 Most scorpion venoms affect sodium channels with prolongation of action potentials, as well as
spontaneous depolarisation of nerves of both adrenergic and parasympathetic nervous systems.
Thus, both adrenergic and cholinergic symptoms occur.
 Hyperkalaemia, hyperglycaemia (with reduction in insulin secretion), and increased secretion of
renin and aldosterone are characteristic of stings by Mesobuthustamulus.
Clinical Features
A. Local
 Rapidly developing, excruciating local pain, swelling,redness, and regional
lymphadenopathy.
B. Systemic
 Signs of autonomic stimulation occur, comprising mydriasis, profuse sweating,
urticaria, excessive salivation, vomiting, parasternal lift, priapism, hypertension,
brady-/tachyarrhythmias, and ventricular premature contractions.
 Pulmonary oedema may develop within 2 to 3 hours leading to death.
 Intracerebral haemorrhage resulting in hemiparesis has been reported.
Convulsions may occur.
 ECG changes: Early changes suggestive of envenomationinclude
o Peaked T waves in leads V2 to V6
o Q waves
o ST-segment elevation in leads I and AVL, and left anterior hemiblock.
 Hyperglycaemia is common with most species.
 Allergic reactions, including anaphylaxis has occurred.
 Palamnaeus species causes local pain, paraesthesias, mild autonomic nervous
system excitation, pulmonary infiltration, eosinophilia, salivation, nausea,
sweating, and mild hypotension.
 Children under the age of 10 are more likely to develop toxicity from most
scorpion stings than older victims. Effects are most severe in infants and toddlers.
Treatment
Most victims (without hypertension or cardiac disease) andchildren over the age of 5 can usually be
handled at home withlocal application of ice and other supportive measures for painrelief. Patients
with cardiac problems/hypertension, elderlyvictims, and children under the age of 5 should be
referred toa hospital for evaluation.
o During transport to hospital
o Immobilise the affected extremity. Do NOT apply tourniquet
o Local application of ice is beneficial in relieving pain.
o A negative-pressure suction device may be used, if available, to extract venom at
approximately 1 atm of negative pressure (it is doubtful whether this really works).
o Do not incise prior to suction.
o On arrival at hospital
o Admit all patients with systemic manifestations (hypertension, hypovolaemia, pulmonary
oedema) to ICU under close monitoring.
o Patients with respiratory failure or with CNS disturbances should be mechanically ventilated.
o Pain may be controlled by paracetamol or morphine tablets.
o Mild to moderate allergic reactions may be treated with antihistamines, with or without
inhaled beta agonists, corticosteroids, or adrenaline. Treatment of severe anaphylaxis must
include oxygen supplementation, airway management, adrenaline, monitoring, and IV fluids.
o Correct fluid and acid-base imbalance. However watch forpulmonary oedema.
o Prazosin hydrochloride acts as an antagonist to scorpion venom, and is also cardioprotective.
The recommended dose is 500 micrograms every 4 to 6 hours for adults, and 250 micrograms
every 4 to 6 hours for children.
o Hypertension (>160/110 mmHg) is conventionally managed with nifedipine at a dose of 10 to
20 mg (adults) or 0.3 mg/kg (children) every 4 to 6 hours.
o Hypotension is treated with dopamine infusion, beginning at a dose of 2 to 5 mcg/kg/min and
increased gradually to 20 mcg/kg/min, to achieve and maintain an SBP of 90 mmHg.
o Pulmonary oedema is treated furosemide (1 to 2 mg/kg IV q4-6 hours) and oxygen.
Life-threatening pulmonary oedema may respond to a nitroprusside drip.
o Agitation and convulsions can be controlled with IV diazepam (5 to 10 mg, adults; 0.2 to 0.3
mg/kg, children; every 10 minutes as required). Phenobarbitone can be given, 5 to 10 mg/kg
o Persistent vomiting responds to metoclopramide 5 to 10 mg IV (adults), or 0.5 mg/kg.
o Cardiac rhythm disturbances are usually transient and resolve without specific treatment in
most of the cases. Persistent tachyarrhythmias can be reversed with propranolol (1 mg/dose
IV, administered no faster than 1 mg/min, repeated every 5 minutes until desired response).
o Antivenom therapy— Scorpion antivenom effective against Mesobuthustamulushas recently
been introduced in India.* The recommended dose is 1 vial (reconstituted in 10 ml of
injection water) initially, followed by further doses if required.
Dog Bites and Other bites(7,29,46–48)
Rabies is an acute viral disease that causes fatal encephalomyelitis in virtually all the warm-blooded
animals including man. The virus is found in wild and some domestic animals, and is transmitted to
other animals and to humans through their saliva (following bites, scratches, licks on broken skin and
mucous membrane). In India, dogs are responsible for about 97% of human rabies, followed by cats
(2%), jackals, mongoose and others (1%).
The disease is mainly transmitted by the bite of a rabid dog. Rabies is endemic in India; so
management of animal bites is essential. Suspect all animal bites, even scratches. Post Exposure
Prophylaxis (PEP) should be started as soon as possible after the bite. Start treatment and observe the
animal for 10 days (applicable only for dog and cat). If the animal (dog and cat) remains healthy
throughout the observation then modify the Post-Exposure Prophylaxis (PEP) to Pre-Exposure
Prophylaxis (PrEP).
Clinical features
Encephalitic (furious) rabies: (80%) fever, hydrophobia, pharyngeal spasms, and hyperactivity
leading to paralysis, coma and death
Paralytic (dumb) rabies: (20%) ascending paralysis, which can mimic Guillain-Barré syndrome.
Paralysis is usually most prominent in the bitten limb, and then spreads symmetrically or
asymmetrically
Factors That Increase the Risk of Infection from an Animal Bite
Bite in extremities with underlying venous Greater than 6 to 12 hours for bites to the
and/or lymphatic compromise arm or leg

Bite involving the hand Greater than 12 to 24 hours for bites to the
face

Bite near or in a prosthetic joint Puncture wounds

Cat bites Victim with diabetes mellitus or

immunosuppressio

Crush injuries Delayed presentation

Indications for Tetanus Prophylaxis

Clean, minor wounds All other wounds

History of tetanus Immune Immune

immunization Vaccine globulin Vaccine globulin

Uncertain or < 3 doses Yes No Yes Yes

≥ 3 doses No, unless > 10 years No No, unless > 5 years No

since last dose since last dose
Management –
WOUND CARE
Wounds should be washed/flushed using a 26 gauge needle and disinfected immediately.
Wounds that are better managed by delayed primary closure after 72 hours
 Deep wounds
 Wounds on the hand and feet,
 More than 12 hours old (24 hours old on face) and
 Puncture wounds
Wounds that can be considered for immediate primary closure
 Clinically uninfected wounds,
 Less than 12 hours old (24 hours on the face)
 Those NOT on the hands or feet
This should be done after thorough cleaning and followed up by antibiotic prophylaxis
(Amoxycillin-clavulanate 625 mg tid x 5 days)
However, most studies do not show any difference in the rates of infection between immediate
suturing and late primary closure.
POST EXPOSURE PROPHYLAXIS
 Pregnancy and infancy are never contraindications to PEP
 Patients who present for evaluation and rabies post-exposure prophylaxis even months after
 having been bitten should be dealt with in the same manner as if the contact occurred
 recently.
 Post-exposure prophylaxis may be discontinued if the animal involved is a dog or cat that
remains healthy for an observation period of 10 days after the exposure occurred
Rabies immunoglobulin (RIG)
Infiltrate into the depth of the wound and around the wound as much as anatomically feasible
of the RIG should be infiltrated around the wound. The remainder, if any, should be injected
at an intramuscular site distant from that of vaccine inoculation e.g. into the anterior thigh
Dose of RIG: 20IU/ kg for Human RIG (HRIG) or 40 IU/ kg of Equine RIG(ERIG)
The total recommended dose should not be exceeded.
If RIG is unavailable on first visit and vaccination has been initiated, its administration can
be delayed by a maximum of 7 days from date of that first injection. If the calculated dose
isinsufficient to infiltrate all wounds, sterile saline may be used to dilute it 2 to 3 fold to
permitthorough infiltration
There are no scientific grounds to perform a skin sensitivity test prior to administrationof ERIG
If RIG is unavailable on 1stvisit its use can be delayed by a maximum of 7days from date of first
vaccine
Intramuscular regimens for rabies PEP
Two intramuscular schedules for category 2 and 3 exposures
 The 5 dose intramuscular regime: one dose of the vaccine should be administered on days
0, 3, 7, 14 and 28 in deltoid region or, in small children, into the antero-lateral area of the
thigh muscle
 The 2-1-1 regimen may also be used. Two doses are given on day 0 in the deltoid muscle,
right and left arm. In addition one dose in the deltoid muscle on day 7 and one on day 21.
Vaccines should NOT be injected into the gluteal region
Post-exposure prophylaxis for previously vaccinated persons
A previously vaccinated person who has had a potential rabies exposure or took preexposure
prophylaxis should receive two intramuscular doses of vaccine; On day 0 or atthe earliest and the
2nd dose 3 days later. Patients who had pre-exposure prophylaxis for rabies should not be given RIG.
 Treatment Algorithm for Rabies

Steps of Post exposure Prophylaxis

Step 1 – Wound wash with soap and
Step 1 water. Wound care
Step 2 – Anti Rabies Vaccination –
Step 2 0,3,7,14,28 im

Treat Other Category III Step 3 – Rabies Immunonoglobulin

animal bites Step 3 with HRIG 20IU/kg or ERIG
and 40IU/kg into wound and around
infectiouos wound
material Step 4
Rabies Category of Step 4 – Observe animal if possible
exposure
Exposure based on exposure for upto 10 days
category Step 1 Others – Antibiotics if need be.

Dog/Cat
Category II Step 2

Step 4

Reassure and
Yes
send home
Reliable
Category I
history Step 1
No
Step 2
 Burns(7,49–52)
Thermal Burns
 First Priority – ABCDE
o Note that children are prone to hypothermia due to its high surface to volume ratio
and low fat mass. Ambient temperature should be from 28° to 32°C (82° to 90°F).
The patient‘s core temperature must be kept at least above 34°C.
 Fluid Resuscitation
Fluid resuscitation is a mainstay in the treatment of burn patients.
Assessment of Burns
o Determination of total Body surface Area The severity of a burn injury is determined
by the total body surface area burned and the depth of the burn. Total body surface
area (TBSA) is an assessed measure of the severity of skin burns.
o In adults, the ―Rule of Nines‖ is used to determine the total percentage of the burned
area for each major section of the body. However, this rule cannot be used in pediatric
burns.
 o An accurate determination of the size of the burned areas is essential to estimate the
amount of intravenous fluids required and the appropriateness of transfer to a burn
unit.
o The degree of burns also is calculated to estimate the prognosis and type of treatment.
o A visual assessment should be made to determine the severity of the burn injuries.
The thickness of the burn – how many layers of skin as well as the amount of other
tissue damaged – is used to classify the degree of the burn. The classification levels of
burns include the following degrees:
 For determining the percentage of body surface area, only partial and full thickness burns are
used.
 Parkland Formula
o Adults
o Ringer‘s lactate - 4 mL × weight (kg) × % BSA burned* over initial 24 h
 Half over the first 8 h from the time of burn
 Other half over the subsequent 16 h
o Example: 70-kg adult with 40% second- and third-degree burns:
 4 mL × 70 kg × 40 = 11,200 mL over 24 h
o Children
o Ringer‘s Lactate- 3mL × weight (kg) × %BSA burned over initial 24 h+ maintenance
 Half over the first 8 h from the time of burn
 Other half over the subsequent 16 h
 Key points of Fluid resuscitation –
o Patients with preexisting cardiac or pulmonary disease require much greater attention
to fluid management. Monitor fluid resuscitation closely by frequent assessment of
vital signs, cerebral and skin perfusion, pulmonary status, and urinary output, as well
as hemodynamic monitoring. Target urine output should be 0.5 to 1.0 mL/kg/h.
o Patients with major burns can quickly receive excessive IV fluid during the ED phase,
particularly if two large-bore peripheral catheters are in place with fluid infusing at a
wide-open rate. Document total fluid infused and titrate infusion to patient response.
o In children weighing <25 kg, a goal urine output of 1.0 mL/kg/h is necessary. Add
5%D to maintenance fluids for children weighing<20 kg due to small glycogen stores.
 Burn History
Once the ABCDs are completed and fluid resuscitation has been initiated, attention should be
focused on obtaining information about the burn history. This should include:
o The patient‘s or EMS provider‘s history of the events,
o Time and place of injury including if the patient was in an enclosed space
o If there was loss of consciousness
 o Causative agent/mechanism of burn
o How long the patient was exposed to the burn source
o If decontamination occurred
o Suspicion of abuse or intentional injury
o Possibility of carbon monoxide intoxication based on history of burns in a closed area
o Presence of facial burns
o Consistency of burn with the history provided
o Allergies and usual medications
o Past medical history including the date of the last tetanus shot
o Patient‘s weight.
 Wound Care –
After evaluation and resuscitation of the patient, attend to burnwounds. Initially wounds are
best covered with a clean, dry sheet. Later,small burns can be covered with a moist saline-
soaked dressing whilethe patient is awaiting admission or transfer.
The soothing effect of coolingon burns is most likely due to local vasoconstriction. Cooling
stabilizesmast cells and reduces histamine release, kinin formation, andthromboxane B2
production. For large burns, sterile drapes are preferred,because application of saline-soaked
dressings to a large area cancause hypothermia.
 ED Care of Minor Burns
o Provide appropriate analgesics before burn care and for outpatient use
o Cleanse burn with mild soap and water or dilute antiseptic solution
o Debride wound as needed
o Apply topical antimicrobial: 1% silver sulfadiazine cream (not on the face or in
patients with a sulfa allergy)
o Bacitracin ointment
o Triple-antibiotic ointment (neomycin, polymyxin B, bacitracin zinc)
o Provide detailed burn care instructions with follow-up in 24–48 h
Dressing should be done twice dailygently removing residual ointment, until healing iscomplete.
Summary of Treatment of Burn -
Chemical Burns –
Unlike thermal burns,chemical burn injuries require tailored evaluations and treatments basedon the
specific agent involved.
Acids tend to cause coagulation necrosis with protein precipitationand form a tough leathery
eschar. The eschar typically limitsdeeper penetration of the agent.
Alkalis produce liquefaction necrosisand saponification of lipids. The result is a poor barrier to
chemicalpenetration and deeper, ongoing burns.
Death early after severe chemical burns is usually related to hypotension,acute renal failure, and
shock as a result of fluid loss. However,systemic toxicity and subsequent morbidity and mortality
may alsooccur if chemicals are absorbed. Acidosis, hypotension, hyperkalemia,dysrhythmia, and
shock can occur with systemic absorption of acids.
The initial management of most chemical burns is -
 Secure ABCDE
 Limit contact with the chemical while ensuring PPE.
 Copiously hydrate the region of contact with normal saline or running water. Almost
universally, earlier irrigation means a better prognosis. Although thermal energy is
produced in an exothermic reaction when using water irrigation, copious amounts of
water will decrease the rate and intensity of the chemical reaction and dissipate the heat.
Continue irrigation at a gentle flow to avoid continued skin contact with chemicals.
 After irrigation and debridement of remaining particles and devitalized tissue, apply
topical antimicrobial agents to affected areas, and provide tetanus immunization.
 Other than measures specific for a particular chemical burn, treatment following initial
therapy is similar to that of thermal burns.
 Phenolic burns can be increased by irrigation with water. Diluted phenol penetrates skin
further than concentrated phenol. Decontamination is more effective by the use of an
undiluted polyethylene glycol solution or isopropyl alcohol. Either irrigation solution
reduces the extent of cutaneous corrosion and also decreases systemic toxicity.
 For ocular burns, at least 1 to 2 L of normal saline for each eye for 30-minute continuous
irrigation is the minimum treatment. Neutralizing substances should not be used.
Electrical Burns and Injuries
Electrical injuries are divided into –
 High-voltage injuries (≥1000 V)
 Low voltage injuries (<1000 V)
 Electric arc flash burns - which by definition do not result in passage of current through the tissue
Types of Electrical injury –
 Standard household electricity is AC
 Electricity in batteries and lightning is DC.
Low frequency (50- to 60-Hz) AC can be more dangerous than similar levels of DC because the
alternating current fluctuations can result in ventricular fibrillation. The identification of electric
shock as due to AC or DC is also important to reconstruct the mechanism of injury. AC current can
produce muscular tetany, during which the victim cannot let go of the electrical source.
Both AC and DC current can hurl the victim away from the current source, which results in severe
blunt force injury.
Clinical Features
System Clinical Features
Cardio-vascular System Asystole/VF
Dysrrhythmias
Neurological System - Occurs CNS –
inapproximately 50% of patients Transient loss of consciousness
with high-voltage injuries as nerve Altered sensorium
tissue has the lowest resistance in Seizures
the body, encouraging electrical Focal neurological deficits
passage Spinal Cord Injury –
Compressive vertebral fractures
MRI can be normal
Deficits can occur days to months after injury with mostly
motor predominance
Peripheral Nerve injury –
Paraesthesia
Peripheral neuropathy
Blunt Trauma Perform FAST to rule out intra-abdominal injury
CT Brain and Cervical Spine
Orthopaedic injury Tetanic muscle contractions
Fractures
Compartment syndrome
Others Muscle injury with rhabdomyolysis leading to AKI
Treatment -
Provide the usual evaluation (airway, breathing, circulation) and resuscitationfor major trauma
victims. Maintain spinal immobilization duringresuscitation until adequate imaging and examination
can be done.
Treat cardiac arrhythmias according to accepted advanced life supportguidelines.
Institute ED cardiac monitoring for patients with highvoltageinjuries and symptomatic
patients.Cardiac complicationsare more common in patients with high-voltage injuries and inthose
with loss of consciousness and include ventricular and atrial dysrhythmias,bradydysrhythmias, and
QT-interval prolongation. Admission for cardiac monitoring is not needed for asymptomatic patients
with normal ECG on presentation after a low-voltage electrical injury.
Assess for tissue damage and identify associated complications. Acareful vascular and neurologic
examination of involved extremities isimportant. Normal findings on initial assessment do not
exclude seriousinjury or the possibility of delayed spinal cord injury following highvoltagecontact.
Focus next on systematic assessment and treatment, especially forinjuries specific to or common in
electrical injury, Fluid resuscitation guided by the Parkland formula (4 mL/kg multipliedby the
percentage of body surface area burned, administered over24 hours) is a reasonable starting point in
fluid management. Extensivedeep tissue damage resulting from high-voltage injury may be present
even when the cutaneous burn seems limited. Therefore, fluid requirementsare often greater than
predicted by the Parkland formula andphysical examination.
Patients with suggestive symptoms or high-voltage injury should bemonitored for the onset of
compartment syndrome, rhabdomyolysis, andrenal failure. If myoglobinuria is suspected;start
aggressive IV fluidresuscitation to maintain a urinary output of 1 and 2 mL/kg/h.
Initial IV rate in the adult is up to 1.5 L/h (more if there is hypotension orobvious blood loss).
Maintain a high urine output
Disposition and follow-up -
••LOW-VOLTAGE INJURIES <600 V
In general, asymptomatic patients who sustain an electric shock of ≤240 V AC can be discharged
home if they have a normal ECG on presentation and normal examination findings. Patients who feel
unwell or have any new ECG abnormality should be monitored for 6 hours.Low-voltage injury
patients with symptoms beyond superficial skin injury or abnormal lab/ECG results may have
systemic injury and require admission as well.
••HIGH-VOLTAGE INJURIES
All patients having contact with ≥600 V AC should be admitted for observation, even if there is no
apparent injury. Routine cardiac monitoring is not required unless the patient is symptomatic or the
initial ECG findings are abnormal.
Patients with extensive cutaneous burns should be transferred to a specialized burn center after initial
trauma stabilization. This is especially true in children.
 Dengue(53,54)

Introduction – Dengue is caused by a virus under the genus Flavivirus. These viruses contain single
stranded RNA and are small in size (50 nm). There are four dengue virus serotypes which are
designated as DENV-1, DENV-2, DENV-3 and DENV4. They are transmitted from an infected
person to others by the bite of the Aedes egyptii female mosquito, the main vector in urbanareas.
Clinically the severity of dengue infection is divided into three categories, i.e., mild, moderate and
severe as shown below.

DHF I and II DHF III and IV

Mangagement of Febrile phase of Dengue / Mild Dengue fever
Management of febrile phase is similar to that of DF. Paracetamol is recommended to keep the
temperature below 39oC. Copious amounts of fluids should be given orally, to the extent the patient
tolerates, oral rehydration solution (ORS), such as those used for the treatment of diarrheal diseases
and/or fruit juices are preferable to plain water. IV fluids should be administered if the patient is
vomiting persistently or refusing to feed. Patients should be monitored for the initial signs of shock.
The critical period is during the transition from the febrile to the afebrile stage and usually occurs
after the third day of illness. Serial hematocrit determinations are essential guide for treatment, since
they reflect the degree of plasma leakage and need for IV administration of fluids. Hematocrit should
be determined daily from the third day until the temperature has remained normal for 1-2 days.
Treatment of Moderate Dengue – DHF I and II
Treatment of Severe Dengue – DHF III
Holiday Segar Formula –
First 10 kg – 4ml/kg/hr
10-20kg – 2ml/kg/hr
>20kg – 1ml/kg/hr
Treatment of Severe Dengue – DHF IV
Organ System involvement–
 Coagulopathy - If the patient has severe thrombocytopenia with active bleeding, it may be
corrected with platelet transfusion. In case of massive hemorrhage, blood should be tested to rule
out coagulopathy. Patients of severe bleeding may have liver dysfunction, and LFTs should be
done. Rarely, I/C bleed may occur in patients with severe thrombocytopenia and coagulopathy.
 Dengue infection may rarely cause acute myocarditis, which may also contribute to the
development of shock. Cardiac complications may be seen in presence of CAD, hypertension,
diabetes and valvular heart disease. Management of shock with IV fluids in this case sometimes
is difficult due to myocardial dysfunction. Patient may develop pulmonary edema.
 Acute tubular necrosis (ATN) may develop and cause acute kidney injury (AKI) if fluid therapy
is not initiated in time. Renal function may be reversible, if shock is corrected rapidly. Urine
output monitoring in dengue infection is therefore very important. Microscopic and macroscopic
hematuria can be found in DHF patients.
Criteria for admission of a patient
Significant bleeding from any site, signs of hypotension, persistent high-grade fever, rapid fall of
platelet count, sudden drop in temperature, he/she should be admitted in hospital. Patients with
evidence of organ involvement and warning signs should also be admitted.
Criteria for discharge of patients
Hospitalized patients who have recovered from acute dengue infection and have no fever for at least
24 hours, normal BP, adequate urine output, no respiratory distress, persistent platelet count
>50,000/mm3 should be discharged from hospital.
Indications for Platelet Transfusion
In general, there is no need to give prophylactic platelets even at < 20000/mm3. Prophylactic platelet
transfusion may be given at level of <10000/mm3in absence of bleeding manifestations. Platelet
transfusion may also be given in prolonged shock with coagulopathy. In case of systemic massive
bleeding, platelet transfusion may be needed in addition to red cell transfusion. Standard dose for
adults is 5-6 units of random donor platelets or 1 unit of apheresis platelets. For neonates/infants, the
dose of platelets should be 10-15 mL/kg of body weight.Use of FFP/cryoprecipitate can be
considered in coagulopathywith bleeding.
Complications -
 CNS involvement - Encephalopathy, encephalitis, febrile seizures, intracranial bleed
 GIT involvement - Acute hepatitis/fulminant failure, cholecystitis, cholangitis, pancreatitis
 Renal involvement - Acute renal failure, hemolytic uremic syndrome, acute tubular necrosis
 Cardiac involvement - Cardiac arrhythmia, cardiomyopathy, myocarditis, pericardial effusion
 Respiratory - Pulmonary edema, ARDS, pulmonary hemorrhage, pleural effusion
 Eye - Conjunctival bleed, macular hemorrhage, visual impairment, optic neuritis
Gastrointestinal Bleed(7,55–58)
Gastrointestinal bleeding is a common problem encountered in the emergency department and in the
primary care setting. Acute or overt gastrointestinal bleeding is visible in the form of hematemesis,
melena or hematochezia. Upper GI bleeding includes hemorrhage originating from the oesophagus to
the ligament of Treitz, at the duodeno-jejunal flexure. Lower GI bleeding is defined as bleeding that
originates from a site distal to the ligament of Treitz.
Clinical Features –
 Upper GI bleeding usually presents with hematemesis (vomiting of fresh blood), ―coffee-ground‖
emesis (vomiting of dark altered blood), and/or melena (black tarry stools).
 Hematochezia (passing of red blood from rectum) usually indicates bleeding from the lower GI
tract, but can occasionally be the presentation for a briskly bleeding upper GI source.
 The presence of frank bloody emesis suggests more active and severe bleeding in comparison to
coffee-ground emesis.
 Variceal hemorrhage is life threatening and should be a major consideration in diagnosis as it
accounts for up to 30% of all cases of acute upper GI bleeding and up to 90% in patients with
liver cirrhosis.
 Lower GI bleeding classically presents with hematochezia, however bleeding from the right
colon or the small intestine can present with melena. Bleeding from the left side of the colon
tends to present bright red in color, whereas bleeding from the right side of the colon often
appears dark or maroon-colored and may be mixed with stool.
 Common symptoms –
o Hemodynamic instability
o Abdominal pain
o Symptoms of anemia- lethargy, fatigue, syncope and angina.
 In general, anatomic and vascular causes of bleeding present with painless, large-volume blood
loss, whereas inflammatory causes of bleeding are associated with diarrhoea and abdominal pain.
Treatment –
 Secure ABCDE
 Start two large bore iv cannula and start resuscitation with iv fluid bolus 20ml/kg 0.9% NS
 Collect samples for CBC, Creat, ECG, ABG, Na+, K+, PT-INR, aPTT, Cross matching,
Grouping
 Antiacids, Somatostatin analogue and analgesic
 If haemorrhage is life threatening, consider activation of massive transfusion protocol and
transfuse O-negative blood.
 Use Blatchford score to risk stratify Upper GI Bleed.
 Notify Surgical on call team within 1 hour of diagnosis and keep patient nil per oral.
Blatchford Score –
Low risk = Score of 0. Any score higher than 0 is
high risk for needing intervention: transfusion,
endoscopy, or surgery.

Summary of Treatment -
ABG Interpretation –(59–61)
The first choice is the radial artery, which is located on the thumb side of the wrist; because of its
small size, use of this artery requires extensive skill in arterial blood sampling. Alternative sites for
access are brachial or femoral arteries, but these have several disadvantages in that they:
 May be harder to locate, because they are less superficial than the radial artery;
 Have poor collateral circulation;
 Are surrounded by structures that could be damaged by faulty technique.
Procedure for Radial ABG -
 Locate the radial artery and perform Allen test if perfusion is doubtful. Once a site is
identified, note anatomic landmarks to be able to find the site again.
 Perform hand hygiene, and inform patient about test and prepare work area and supplies.
 Disinfect the sampling site on the patient with 70% alcohol and allow it to dry.
 Assemble the needle and draw heparin to the requiredlevel.
 Holding the syringe and needle like a dart, use the index finger to locate the pulse again,
inform the patient that the skin is about to be pierced then insert the needle at a 45 degree
angle, approximately 1 cm distal to the index finger, to avoid contaminating the area.
 Advance the needle into the radial artery until a blood flashback appears, then allow the
syringe to fill to the appropriate level. DO NOT pull back the syringe plunger.
 Withdraw the needle and syringe; place a clean, dry piece of gauze or cotton wool over the
site and have the patient apply firm pressure for sufficient time to stop the bleeding. Check
whether bleeding has stopped after 2–3 minutes. Do not immediately apply tape to hold gauze
in place as it doesn‘t offer adequate pressure to stem bleeding.More time may be needed for
patients who have high blood pressure or are taking anticoagulants.
 Use a one-hand scoop technique to recap the needle after removal or discard needle.
 Expel air bubbles, cap the syringe and roll the specimen between the hands to gently mix it.
Cap the syringe to prevent contact between the sample and the air, and to prevent leak.
 Label the sample syringe and dispose all used material and gloves.
 Wash hands thoroughly with soap and water or alternatively, use alcohol rub solution.
 Check the patient site for bleeding and thank the patient.
 Transport the sample immediately to the laboratory.
Preanalytical errors are caused at the following stages:

During Preparation During sampling/handling During Storage

Missing or wrongpatient
identification
Anticoagulant Issues –
 Use of the incorrect type or
amount of anticoagulant
 Dilution due to use of liquid
heparin
 Insufficient amount of heparin
 Binding of electrolytes to
heparin
Mixture of venous and arterial Incorrect storage
blood during puncturing
Air bubbles in the sample. Any Hemolysis of blood cells
air bubble in the sample must be
expelled as soon as possible
after withdrawing the sample.
An air bubble whose relative
volume is up to 1% of the blood
in the syringe is a source of
significant error and seriously
affects pO2.

General Storage Recommendation

 Analyze within 30 min. For samples with high paO2 e.g., shunt or with high leukocyte or
platelet count also analyze within 5 min.
 When analysis is expected to be delayed for more than 30 minutes, use ice slurry
 During preparation prior to sample transfer visually inspect the sample for clots.
 Insufficient mixing can cause coagulation of the sample. It is recommended to mix the blood
sample thoroughly by inverting the syringe 10 times and rolling it between the palms as
shown in Figure 1. This prevents stacking (such as coins or plates) of red blood cells.
Anticoagulation Use - Liquid heparin
The use of liquid heparin as the anticoagulant causes a dilution of the sample, i.e., dilutes the plasma,
but not the contents of the blood cells. As a consequence, parameters such as pCO2 and electrolytes
are affected. Only 0.05 mL of heparin is required to anticoagulate 1 mL of blood. Dead space
volume of a standard 5 mL syringe with 1 inch 22 gauge needle is 0.2 mL; filling the syringe dead
space with heparin provides sufficient volume to anticoagulate a 4-mL blood sample. If smaller
sample volumes are obtained or more liquid heparin is left in the syringe, then the dilution effect will
be even greater. The dilution effect also depends on the hematocrit value.
Plasma electrolytes decrease linearly with the dilution of plasma with pCO2, Glucose, and Hb.
pH and pO2 values are relatively unaffected by dilution. paO2 is only as little as 2% of the oxygen
physically dissolved in the plasma, and so the oximetry parameters are unaffected.
Heparin binds to positive ions such as Ca2+, K+, and Na+. Electrolytes bound to heparin cannot be
measured by ion-selective electrodes, and the final effect will be measurement offalsely low values.
The binding effect and inaccuracy of results are especially significant for correctedCa2+.
Interpretation
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