Acute Biologic CriSiS

Arlene D. LAtorre
 Acute Biologic Crisis
• Condition that may result to patient mortality
if left unattended in a brief period of time
• Condition that warrants immediate attention
for reversal of disease process and prevention
of further morbidity and mortality
Conditions that can be considered ABC
• Heart failure & dysrhythmias
• Respiratory Failures & Acute Respiratory
Distress Syndrome
• Burns
• Hepatic coma
• DKA/HHNK
• Thyroid Crisis & Adrenal Crisis
• Multi System Organ Failure & Shock
 Coronary Artery Disease & Acute
Coronary Syndromes
• Most common cause of cardiovascular
disability and death
• It refers to a spectrum of illnesses that range
from the least life threatening to the most life
threatening acute coronary syndrome ( AMI/
Heart attack)
 CAD & Acute Coronary Syndrome
• Incomplete occlusion of the coronary arteries
lead to Angina ( Ischemia)
• Complete occlusion of the coronary arteries
lead to myocardial Infarction
• The heart will pump harder to meet the O2
demand leading to Congestive Heart Failure
 Non Modifiable Risk Factors of
CAD/ACS
• Age
• Gender
• Race
• Heredity
Modifiable Risk Factors of CAD/ACS
• Stress
• Diet
• Exercise
• Cigarette Smoking
• Alcohol
• Hypertension
• Hyperlipidemia
• Diabetes Mellitus
• Obesity
• Personality Type or Behavioral Factors
• Contraceptive Pills
 Cardiovascular Assessment
• Chest Pain
– Most common
– Due to Ischemia or MI
– Precipitated by stress or can be relieved by
Nitroglycerin (NTG)
– In MI, it is more intense, unrelated to activities
and can’t be relieved by NTG
– If it occurs during breathing, suspect respiratory
problems
 Rough diagram of pain zones in MI ( dark red = most
typical area, light red=other possible areas, view of the
chest
 Cardiovascular Assessment
• Dyspnea
– Subjective feeling ( inability to get enough air)
– Dyspnea on exertion is due to increased O2
myocardial demand
– Orthopnea is related to blood pooling in the
pulmonary bed; suspect Pulmonary edema
– Any sudden or acute dyspnea may be a sign of
pulmonary embolism
Tightness of the chest
• Cough / sputum
– Mucoid and foamy sputum can be a sign of CHF
– Whitish – viral infection
– Pink – tinged or rusty frothy appearance may
signal Pulmonary edema
– Change in color other than above mentioned may
signify infection
• Cyanosis
– Bluish discoloration of the skin and mucous
membrane
– O2 saturation is below 90%

• Fatigue
– May be due to anemias or related to decreased
cardiac output
• Palpitations
– Awareness of rapid or irregular heartbeat
– Autonomic Nervous System and Adrenal Glands
response ( stress)
• Syncope
– Transient loss of consciousness
– Due to decreased cerebral tissue perfusion
• Edema
– Due to: Increased Hydrostatic pressure (HP)
– Decreased Colloidal Oncotic pressure (COP)
– Obstructed Lymphatic or Vascular System
– Related to Inflammatory reaction
 Types of Edema
• Bilateral edema
– CHF or Reanal failure
• Unilateral Edema
– Vascular or Lymphatic Obstruction
• Non-pitting edema
– Inflammatory
• Pitting edema
– HP and COP derangement
• Skin
– Color, temperature, hair growth, nails, capillary
refill
– Spooning of fingers / clubbing of fingers
Clubbing of fingers
• Heart rate - 60-100
• Rhythm – regular or irregular
• Bruits and Thrills – murmurlike; vascular in
origin
– Palpate a thrill, auscultate a bruit
• Blood pressure
• Jugular venous pressure
• Cardiac rate and rhythm
• Tachycardia = > 100 beats /min
• Bradycardia = < 60 beats / min
• Arrhythmias = irregular rate and rhythm
• S1 – closure of AV valves (lub)
• S2 closure of SL valves (dub)
• S3 & S4 diastolic filling sound
• S3 heard after S2
– If present suspect CHF; common
• S4 is heard prior to S1: if present suspect non-
compliant ventricles although this is common
among the elderly.
• Murmurs – turbulence of blood flow; if
positive watch out for FVE; normal until 1 year
old
• Pericardial Friction Rub –” squeaking sound”
suspect pericardial effusion if this is heard
• Muffled Heart Sounds – if positive rule out
Cardiac Tamponade and other similar
problems like effusion
 Laboratory & Diagnostic Tests
• Complete blood count – RBC suggest tissue
oxygenation
– Elevated WBC may indicate infectious heart
disease and MI
• Erythrocyte Sedimentation Rate (ESR) – is
elevated in infectious heart disorder or MI
• Normal range: Males 15-20 mm/hr
• Females : 20-30 mm/hr
• Blood Coagulation Test:
• 1. Prothrombin Time (PT,Pro Time) – It
measures time required for clotting to occur.
Used to evaluate effectiveness of COUMADIN.
Normal range 11-16 secs.
• 2. Partial Thromboplastin Time (PTT)- best
screening test for disorders of coagulation.
Used to determine the effectiveness of
HEPARIN. Normal range: 60-70 secs
• Blood Urea Nitrogen (BUN) – Indicator of
renal function
• Normal range: 10-20 mg/dl ( 5-25 mg/dl is
also accepted)
• Blood Lipids:
• 1. Serum cholesterol: 150 mg/dl
• 2. Serum Triglycerides: 140-200 mg/dl
• Serum Enzymes Studies:
• 1. Aspartate Aminotransferase ( AST) –
elevated level indicates tissue necrosis.
Normal range: 7-40 muml
• 2. CK-MB – elevated 4-6 hours from onset of
infarction; peaks 24-36 hours. Returns to
normal 4-7 days
• Normal range: Males 50-325 mu/ml; Females:
50 to 250 mu/ml
• 3. Lactic Dehydrogenase (LDL) – Onset: 12
hours Peak: 48 hours; returns to normal: 10-
14 days
• 4. Hydroxybuterate Dehydroxynase (HBD)-
valuable in detecting silent MI because it ia
elevated for a long period of time
• ONSET: 10- 12 HOURS: Peaks: 48-72 hrs;
Returns to Normal 12 – 13 days
• 5. Troponin – Most specific lab test to detect
MI..Troponin has 3 compartments: I, C and T
• Troponin 1 persist for 4 – 7 days.
• Serum Electrolytes/ Blood Chemistry:
• 1. Sodium ( Na)
• 2. Potassium (K)
• 3. Calcium ( Ca)
• 4. Magnesium ( Mg)
• 5. Glucose
• 6. Glycosylated Hemoglobin ( Hemoglobin A)
 Diagnostic Test
• Hemodynamic Monitoring
– Swan Ganz Catheterization
• Right side of the heart
• Pulmonary artery pressure
• Pulmonary artery occlusive pressure
• Right atrial pressure
• Cardiac Output
• Goal:
• Pain relief
• Reduction of myocardial oxygen consumption
• Prevention and treatment of complications
 Intervention
• Admit to the CCU/ICU
• Activity
– Day 1: bed rest, if stable
– Day 2-3: bed rest, but patient may be allowed to
sit on chair fro 15 – 20 minutes
– Early mobilization is recommended for
uncomplicated AMI
 Intervention
• Monitoring Vital signs
– First 6 hours – q30-60 mins
– Next 24 hours –q2 hours
– Thereafter q4 hours
Diet
NPO: 1st 24 hours
If stable low salt, low cholesterol
 Intervention
• IV Fluids
– D5W to KVO
– If unable to take food/fluid per orem
– 1000ml/8 hours
– K supplement
 INTERVENTION
• Pain Medication
– Morphine So4 ( 2-5mg/IV dose)
– Potent analgesic
– Peripheral venous dilation
– Pulmonary venous distention
– Inferior wall MI: may increase vagal discharge
• Tranquilizers
– To decrease anxiety
– Diazepam (5-10 mg per IV/orem)

• Laxative
– To prevent straining during defecation
– Lactulose ( HS)
 Drugs to limit Infacrt size
• Beta Blockers
– Hyperdynamic states, Hpn w/o evidence of heart
failure
– Reduce myocardial oxygen consumption by
decreasing BP, heart rate, Myocardial Contractility
& Calcium output
– Ex: Propanolol, Metoprolol, Atenolol
 Nursing Consideration:
• 1. Assess pulse rate before administration;
withhold if bradycardia is present
• 2. Administer w/ food, may cause GI upset
• 3. Do not administer w/ asthma, it causes
bronchoconstriction
• 4. Do not give to patient w/ DM, it causes
hypoglycemia
• 5. Antidote for Beta Blocker poisoning is
GLUCAGON
• Nitrates
• Act by augmenting perfusion at the border of
the ischemic zone
• Generalized vasodilation
• Reducing myocardial O2 demand
– Lowering preload
– Lowering afterload
• Ex. IV Nitroglycerine, sublingual nitroglycerine,
Oral/transdermal Nitroglycerine
ACE inhibitors (Angiotensin Converting Enzyme)
1. Reduce mortality rates after MI.
2. Administer ACE inhibitors as soon as possible
3. ACE inhibitors have the greatest benefit in patients
with ventricular dysfunction.
4. Continue ACE inhibitors indefinitely after MI.
5. Angiotensin-receptor blockers may be used as an
alternative
6. Adverse effects, such as a persistent cough,
• ACE inhibitors are meds that slow (inhibit) the
activity of the enzyme ACE which decreases
the production of angiotensin II . As a result ,
blood vessels enlarge or dilate, & blood
pressure is reduced.
 Nursing Considerations:
• 1. Only a maximum of 3 doses at 5 min interval of
NTG
• 2. Offer sips of water before giving it sublingually
• 3. Store the medication in a cool, dry place; use
dark / amber container
• 4. If side effects is noticed, do not discontinue the
drug. This is usual in the first few doses of
medication
• 5. Rotate skin sites for nitro patch
Aspirin and/or antiplatelet therapy

1.Continue aspirin indefinitely

2.Clopidogrel may be used as an

alternative only if resistance or allergy
to aspirin.
• Nursing Considerations:
• 1.Assess for signs and symptoms of Bleeding.
• 2.Avoid straining at stool to avoid rectal bleeding.
• 3.It should be given with food.
• 4.Observe for toxicity- Tinnitus (ringing of ears).
• 5.May cause Bronchoconstriction- Observe
for wheezing.
•
Heparin
1. Assess for S/S of Bleeding.

2.Keep Protamine Sulfate available.

3. If used SQ. do not aspirate to prevent hematoma

formation.

4. Monitor for PTT or APTT

5. Used for a maximum of 2 weeks.

•
Coumadin (Warfarin Sodium)
1. Assess for bleeding
2. Keep Vitamin K available.
3. Monitor for Prothrombin Time
4. Do not give together with aspirin to prevent
bleeding.
5. Minimize green leafy vegetables inthe diet.
Thombolytic therapy
The effectiveness:
> highest in the first 2 hours
>After 12 hours, the risk associated with
thrombolytictherapy outweighs any benefit
contraindicated
unstable angina I
• and for the treatment of individuals with evidence
of cardiogenic shock
streptokinase,urokinase, andalteplase(recombinant
tissue plasminogen activator ,
rtPA),reteplase,tenecteplase
•
 Surgical Care
• Percutaneous Transluminal Coronary Angioplasty
• -treatment of choice
• PCI provides greater coronary patency

• lower risk of bleeding

• and instant knowledge about the extent of the underlying

disease.

• A specially designed balloon – tipped catheter is inserted

under flouroscopic guidance and advance to the site of the
obstruction.
•
 Intravascular stenting
•
Biologic Stent is produced throughcoagulation of
collagen, ellastin andother tissues in the vessel
wall by laser, photocoagulation or radio
frequency.
•
• It is done to prevent restenosis
after Percutaneous Transluminal
CoronaryAngioplasty.
•
•
Emergent or urgent
• coronary artery graftbypass surgery
• (CABG)is indicated
•
• angioplasty fails
•
• Severe narrowing of 1or more coronary artery.
•
• Commonly used: Saphenous vein and internal mammary
artery.
•
 Complications
• Inflammation
• Mechanical
• Electrical Abnormalities
 Cardiac Rehabilitation
• A process which a person restored to healthand
maintains optimal physiologic, psychosocial and
recreational functions.
•
• Begins with the moment a client is admitted to
the hospital for emergency care, it continues for
months and even years after the client is
discharged from the health care facility.
•
 Goals of Rehabilitation:

• 1. To live as full, vital and productive life

as possible.
• 2. Remain within the limits of the hearth’s
abilityto respond to activity and stress.
• Activities:

• 1. Exercise may gradually implementedfrom the

hospital onwards.

• 2. Exercise session is terminated if anyone of the

following occurs: cyanosis,cold sweats, faintness,
extreme fatigue,severe dyspnea, pallor, chest
pain, PR more than 100/ min.,
dysrhythmiasgreater than 160/95mmHg.
• Teaching and Counseling

Self management education guide.

Control hypertension with continued medical supervision.

Diet
Weight reduction program

Progressive exercise

Stress management techniques

Resumption of sexual activity after 4-6 weeks from discharge, if

appropriate.
Teaching guide on resumption of sexual activities:

1. Assume less fatiguing position.

2. The non- MI partner take the active role

3. Take nitroglycerine before sexual activity

4. If dyspnea, chest pain or palpitations occur,moderation

should be observed; if symptom persist stop sexual activity.

5. Develop other means of sexual expression

• Thyroid storm :Thyroid crisis:
thyrotoxicosis – life threatening occurring in
extreme hyperthyroidism. Usually occurs in
clients w/ a long term untreated
hyperthyroidism or in clients experiencing a
stressor such as infection, trauma or
manipulaton or unprepared surgery of the
thyroid gland.
S/SX include:
• Hyperthermia >102F (39C)- initial sign
• Systolic Hypertension
• Dysrrhytmias
• Delirium , diarrhea, tremors
• Nausea, Vomiting and abdominal pain
• Tachyarrythmia
• >Bp, >RR
 Thyroid Storm/ Thyrotoxicosis
= An acute LIFE-threatening health condition that is
associated with untreated hyperthyroidism
characterized by excessive thyroid hormone.
During thyroid storm, an individual’s heart rate,
blood pressure & body temp can soar to
dangerously high levels. Without prompt ,
aggressive tx, thyroid storm can be fatal.
• 2 Essential thyroid hormones:
• 1. T3 – triiodothyronine
• 2. T4 - thyroxine
• - these control the rate at which every cell in
your body works ( metabolism)
CAUSEs:
1. Severe untreated hyperthyroidism
2. Untreated overactive thyroid gland
3. Manipulation f the thyroid during surgery
causing the release of excessive hormones
in the blood
4. Infection associated with hyperthyroidism
• People with hyperthyroidism may develop
thyroid storm after experiencing one of the ff:
• Trauma
• Surgery
• Severe emotional stress
• Stroke
• DKA
• CHF
• Pulmonary Embolism
 Thyroid Storm S/Sx
• 1. Racing heart rate ( tachycardia) that
exceeds 140 beats per minute
• 2. Atrial Fibrillation
• 3. High fever
• 4. Persistent sweating
• 5. Shaking
• 6. Agitation
• 7. Delirium and coma
• 8. Severe vomiting and diarrhea
• 9. Restlessness, confusion and
Seizures
 DX
• = same as hyperthyroidism but they are more
sudden, severe & extreme.
• < TSH ; > T3 > T4
• NV;
• TSH – 0.4 to 4 mlU/L
 MX
• 1. PTU = Propylthiouracil
• 2. Tapazole = Methimazole
• = to reduce the production of T3 T4
• = radioactive iodine which destroys the thyroid
• = Avoid taking iodine in lieu of medical tx , as this can
worsen the condition
• = If thyroid hormone is destroyed by radioactive iodine
tx or removed surgically, you will need to take synthetic
thyroid hormone for the rest of your life
• = Pregnant women who have hyperthyroidism can’t be
treated with radioactive iodine because it would harm
the unborn child. In those cases, a woman’s thyroid
would be removed surgically.
 DISORDERS OF the THYROID GLAND
NURSING INTERVENTIONS
• 1. Maintain PATENT airway and
adequate ventilation
• 2. Administer anti-thyroid
medications such as Lugol’s
solution, Propranolol, and
Glucocorticoids
 ANTI-Thyroid Medications

ANTI-THYROID medications
Lugol’s Solution
• Used to decrease the vascularity of the
thyroid
• T3 and T4 production diminishes
• Given per orem, can be diluted with juice
• Use straw
 DISORDERS OF the THYROID GLAND

NURSING INTERVENTIONS
• 3. Monitor VS
• 4. Monitor Cardiac rhythms
• 5. Administer PARACETAMOL ( not
Aspirin) for FEVER
 DISORDERS OF the THYROID GLAND

NURSING INTERVENTIONS
• 6. Manage Seizures as required.
• 7. Provide a quiet environment
 MyxEDEMA COMA
• Is a state of decompensated hypothyroidism
• = A person may have lab values identical to a
normal hypothyroid state, but a stressful event (
infection, MI or stroke) precipitates myxedema
coma state, usually in the elderly.
• Myxedema coma is a loss of brain function as a
result of severe, longstanding low level of thyroid
hormone in the blood. It is considered life
threatening complication of hypothyroididm
 Precipitating factors
• 1. Burns
• 2. CO2 retention
• GI hemorrhage
• Hypoglycemia
• Hypothermia
• Infection ( pneumonia, Influenza, sepsis)
• Medications ( Amiodarone, Anesthesia, Barbiturates,
Betablockers, Diuretics, Lithium, Narcotics,
Phenothiazines, Phenytoin, Rifampicin, Tranquilizers)
• Stroke
• Surgery
• Trauma
 Assessment:
• 1. Altered mentation
• Alopecia
• Bladder dystonia & distension
• Cardiovascular – elevated diastolic pressure
(early)
• Hypotension ( late)
• Bradycardia
• Delayed reflex relaxation
• Dry, cool doughy skin
• GI:
• < motility
• Abdominal distension
• Paralytic ileus
• Fecal impaction
• Myxedema megacolon – late
• Hypothermia
• Hyperventilation
• Myxedematous face:
• Generalized swelling
• Macroglossia
• Ptosis
• Priorbital edema
• Coarse, sparse hair
 TX
• ICU
• Hormone Replacement
• IV levothyroxine (T4) as opposed to IV
Iiothyronine (T3)
• - Hydrocortisone should be administered until
co-existing adrenal insufficiency is ruled out
 Addisonian CRISIS ( Acute Adrenal
Crisis)
• Is a serious medical emergency caused by
extremely low levels of cortisol. Cortisol is an
important hormone produced by the adrenal
glands & is normally released as part of the
body’s response to stress. People with
Addison’s disease are at greater risk of
developing an Addisonian crisis.
DISORDERS OF the ADRENAL GLAND

Hypo-secretion: ADDISON’S Disease

• Decreased secretion of adrenal
cortex hormones, especially
glucocorticoids and
mineralocorticoids
• CAUSE: tumor, idopathic
 DISORDERS OF the ADRENAL GLAND

PATHOPHYSIOLOGY
• Decreased Glucocorticoids
decreased resistance to stress
 S/Sx
• 1. Extreme weakness
• 2. Mental confusion
• 3. Darkening of the skin
• 4. Dizziness
• 5. Nausea or abdominal pain
• 6. Vomiting
• 7. Fever
• 8. a sudden pain in the lower back or legs
• 9. anorexia
• 10. extremely low blood pressure
• 11. chills, sweating, skin rashes, tachycardia, loss oc consciousness
• ** some people have a craving for salt
 DISORDERS OF the ADRENAL GLAND

ASSESSMENT Findings for Addison’s

disease
• 1. Weight loss
• 2. GI disturbances
• 3. Muscle weakness, lethargy and
fatigue
• 4. Hyponatremia
 DISORDERS OF the ADRENAL GLAND

ASSESSMENT Findings for Addison’s

disease
• 5. Hyperkalemia
• 6. Hypoglycemia
• 7. dehydration and hypovolemia
• 8. Increased skin pigmentation
• Causes of Addison’s disease:
• 1. prolonged use of glucocorticoids such as
prednisone
• 2. Severe infections, including fungal & viral
infections
• 3. tumors
• 4. extensive use of blood thinners that help
prevent blood clots
• 5. Surgery on the adrenal gland
 DISORDERS OF the ADRENAL GLAND

• NURSING INTERVENTIONS
• 1. Monitor VS especially BP
• 2. Monitor weight and I and O
• 3. Monitor blood glucose level and K
• 4. Administer hormonal agents as
prescribed
 DISORDERS OF the ADRENAL GLAND
• NURSING INTERVENTIONS
• 5. Observe for ADDISONIAN crisis
• 6. Educate the client regarding lifelong
treatment, avoidance of strenuous
activities, stress and seeking prompt
consult during illness
DISORDERS OF the ADRENAL GLAND

NURSING INTERVENTIONS
• 7. Provide a high-protein, high
carbohydrate and increased
sodium intake
 DISORDERS OF the ADRENAL GLAND

ADDISONIAN crisis
• A life-threatening disorders caused
by acute severe adrenal
insufficiency
CAUSES: Severe stress, infection,
trauma or surgery
DISORDERS OF the ADRENAL GLAND

ADDISONIAN crisis
PATHOPHYSIOLOGY
• Overwhelming stimuli mobilize
body defense decreased stress
hormones inadequate coping
 DISORDERS OF the ADRENAL GLAND

ASSESSMENT Findings for Addisonian Crisis=

“severe lahat”
• 1. Severe headache
• 2. Severe pain
• 3. Severe weakness
• 4. Severe hypotension
• 5. Signs of Shock
 DX Of Addisonian Crisis
• ACTH – adrenocorticotropic hormone
measurement in the blood
 TX for Addison’s
• - immediate injection of hydrocortisone
(IV/IM)
 DISORDERS OF the ADRENAL GLAND

NURSING INTERVENTIONS
• 1. Administer IV glucocorticoids, usually
hydrocortisone
• 2. Monitor VS frequently
• 3. Monitor I and O, neurological status,
electrolyte imbalances and blood
glucose
 DISORDERS OF the ADRENAL GLAND

NURSING INTERVENTIONS
• 4. Administer IVF
• 5. Maintain bed rest
• 6. Administer prescribed antibiotics
 Diabetic Ketoacidosis (DKA)
• is a life threatening acute insulin resulting in
metabolic acidosis from ketone bodies (acid
end product of breakdown of fats ); it can be
triggered by emotional stress,
uncompensated exercise, infection, trauma,
or insufficient or delayed insulin
administration.
 Causes:
• Causes may include inadequate secretion of
endogenous insulin
• Insufficient exogenous insulin
• Increased insulin requirements ( due to
physical or emotional stress)
• Medications that interfere with insulin
secretion or action
 Patho
1. Normally, insulin breaks down glucose. In
diabetes, there is inadequate, so glucose is not
metabolized properly & subsequently builds up in
the blood ( causing hyperglycemia)
2. Exogenous insulin is the only way to metabolize
glucose
3. Eventually, the body uses fat for energy because
it is unable to use glucose, the body’s primary
energy source.
• 4. Fat metabolism yields ketone bodies, an
acid end-product; the person is then in a state
of ketosis
• 5. As ketones build up in the blood, acidosis
occurs
• 6. Acidosis worsens as blood glucose levels
rise & more ketones accumulate
 Sx of acidosis
1. Polyuria ( as osmotic diuresis occurs from
renal perfusion w hyperglycemic blood)
2. Polydipsia ( as extreme dehydration occurs)
3. Hypokalemia
4. Kussmaul’s respiration
5. Ketonuria
6. Dizziness
 Nursing Interventions
• 1. Administer regular insulin, as ordered
• 2. Monitor serum glucose levels as insulin is given
• 3. Monitor K levels, because K shifts affect the
heart
• 4. Monitor respirations, because respiratory
distress can occur
5. Replace fluids
6. Monitor blood gas studies to check the
progression of acidosis
• life threatening severe hyperglycemia (
without ketoacidosis) & hypertonic
dehydration usually occurring with DM
type 2 triggered by a variety of
situations eg. medications, infection,
acute illness, invasive procedure or a
chronic illness.
• = results from reactive insulin deficiency
 Causes
• = Inadequate insulin secretion or action
• = increased insulin requirement associated
with stress
• Also ingestion of the ff:
• > Thiazide diuretics
• > Glucocorticoid
• >Phenytoin ( anticonvulsant)
• > Chlorpromazine ( Thorazine)
 Patho
• 1. Blood glucose levels rise; although some
insulin is present; there is not enough to bring
serum glucose levels to normal
• 2. Acidosis does not occur because the body
secretes enough insulin to avoid fat
metabolism ( therefore there are no ketones
present) but not enough to use glucose
properly
• 3. As a result of hyperglycemia, glycosuria &
polyuria ( from osmotic diuresis) occur
• 4. Polyuria causes dehydration of the
extracellular & intracellular spaces, leading to
Neurologic changes
• Risk of developing HHNK/HONK is higher if you:
• 1. have Type 2 DM – if you don’t monitor your
blood sugar or you don’t yet know you have type
2 DM
• 2. Older than age 65
• 3. Have another chronic health condition ( CHF,
kidney disease)
• 4. Have an infection such as pneumonia, UTI ( w/c
causes blood sugar levels to rise
• 5. Taking certain meds..ex, prednisone, diuretics,
dilantin
 Assessment of HHNK/HHS
• 1. Plasma glucose levels > 600mg/dl
(30mmol/L)
• 2. Serum osmolality >320 mosm/kg
• 3. Profound dehydration,
 Increased Intracranial pressure ( >14
mm/Hg)
CLINICAL MANIFESTATIONS
Early manifestations:
• Changes in the LOC- usually the earliest
• Pupillary changes- fixed, slowed response
• Headache
• vomiting
 Increased Intracranial pressure
CLINICAL MANIFESTATIONS
late manifestations:
• Cushing reflex- systolic hypertension,
bradycardia and wide pulse pressure
• bradypnea
• Hyperthermia
• Abnormal posturing
 Increased Intracranial pressure

Nursing interventions:
Maintain patent airway
• 1. Elevate the head of the bed 15-30 degrees-
to promote venous drainage
• 2. assists in administering 100% oxygen or
controlled hyperventilation- to reduce the CO2
blood levelsconstricts blood
vesselsreduces edema
 Increased Intracranial pressure
Nursing interventions
• 3. Administer prescribed medications- usually
– Mannitol- to produce negative fluid balance
– corticosteroid- to reduce edema
– anticonvulsants-p to prevent seizures
 Increased Intracranial pressure
Increased Intracranial pressure
Nursing interventions
• 4. Reduce environmental stimuli
• 5. Avoid activities that can increase ICP like
valsalva, coughing, shivering, and vigorous
suctioning
 Increased Intracranial pressure
• Nursing interventions
• 6. Keep head on a neutral position. AVOID-
extreme flexion, valsalva
• 7. monitor for secondary complications
– Diabetes insipidus- output of >200 mL/hr
– SIADH
 RETINAL DETACHMENT
• Separation of the retina (epithelium and
rods/cones)
– Tear in the retina allows vitreous humor to seep
• Cause: trauma, glaucoma, hemorrhage, tumor,
inflammation, cataract surgery, diabetic retinopathy
• s/sx: floating, spots, flashes of light, curtain vision,
cobwebs, painless loss of vision, scotoma, veil
occurs in the vision
Layers
– Sclera
– Choroid
– Retina
• Inner-rods/cones
• Outer-epithelium
• Management: cover the eyes, dependent position, bed rest,
ophthalmoscopy to dx
• Surgery:
– Scleral Buckling: shortening of the sclera
– Cryosurgery or diathermy: heat or cold (promote healing)
– Photocoagulation: light beam/argon laser (promote healing)
Postop care: position on the unaffected, pressure patch, avoid
activity that may increase ITP and IAP, 6 weeks full recovery
HEMORRHAGE-common complication
– Eye shield at night (4 weeks), no reading for 3 weeks, eye drop
administration
Adult Respiratory Distress Syndrome ARDS

• By nature it is also Pulmonary Edema

• It can quickly lead to Respiratory Failure if
not managed immediately (48 hours)
• Other name:
• Shock Lung
• Stiff Lung
• Wet Lung
• Da Nang Lung
 ARDS
• Any condition that increases alveolocapillary
permeability would be considered to be
Risk factors:
• Anaphylaxis
• All types of Lung Embolism
• Pneumonia
• Tuberculosis
• CHF
 ARDS
• ↑ alveolocapillary permeability
• ↓
• fluids then accumulates in
• the lung interstitium
• (between capillaries and alveolar sacs)
• ↓
 fluids also penetrate the
alveolar spaces and small airways
↓
bibasilar crackles may be heard on auscultation
pink frothy sputum
↓surfactant production to atelectasis
↓blood flow allows platelets to aggregate → (serotonin,
bradykinin, histamine activation)
↑capillary permeability
↓
Gas Exchange will be impaired
• Manifestations:
1. Initial
rapid, shallow breathing with dyspnea
Bibasilar crackles and rhonchi
↓LOC
Pink frothy sputum
2. Late
Retraction of ICS
severe hypoxemia
Hypotension
↓urine output
Acidosis
Arryhthmias
 ARDS
Diagnostic and Laboratory Tests
• Identify the risk factors
(sputum C&S, blood cultures etc.)
• ABG
• Pulmonary Artery Catheterization
• Serial Chest x-rays
 ARDS
Management:
• Treat the cause and prevent hypoxemia.
• ETT with mechanical ventilator PEEP may be added
• Sedatives and Narcotics to minimize restlessness
• Vecuronium (neuromuscular blocking agent)
• Steroids to reduce inflammation
• NaHCO3 to reverse Acidosis
• Fluids and vasopressors to maintain blood pressure
• Antibiotics
 ARDS
• A-acute attack to the pulmonary system
• R-respiratory arrest is very imminent
• D-diminished gas exchange, derangement in
V/Q ratio
• S-symptoms may be silent, secretion of
surfactant is reduced, sputum (pink and
frothy)
 RESPIRATORY ARREST
• ACUTE RESPIRATORY FAILURE
– Life threatening
– No gas exchange
– Pa02 is less than 50 mm Hg
– PaC02 is above 50 mm Hg
– Arterial pH is below 7.35
– Ventilation or Perfusion is impaired (V/Q)
 Acute Respiratory Failure
• Cause:
– Decreased respiratory drive
– Dysfunction of chest wall
– Dysfunction of lung parenchyma
– Example: Brain and spinal injury, multiple
sclerosis, ALS, GBS, poliomyelitis, muscular
dystrophy, sedatives, anesthetic, pleural effusion,
pneumonia, status asthmaticus, atelectasis,
pulmonary embolism, pulmonary edema, ARDS
 Acute Respiratory Failure
• S/sx: restlessness, dyspnea, headache,
increased RR, HR, BP;
– Lethargy, cyanosis, decompensatory
– Respiratory distress, no lung sound
Dx: rule out the cause
ABG, pulse oximetry, v/s, respi assessment
Management: intubate and attached to mech vent.
 HEMORRHAGE
• Stop the bleeding
– Elevate (optional)
– Pressure
• Site
• Proximal
• Torniquet
• Note: Pain, Pallor, Paralysis, Paresthesia,
Poikilothermia
• ssess 5 p’s distal
 torniquet
• Assess
– Venous bleeders
– Dark red
– Oozing
– Apply torniquet snugly
– Arterial bleeders
– Bright red
– Spurting
– Apply torniquet tightly and release every 15 min
• Esophageal bleeders
– SENGSTAKEN BLAKEMORE TUBE
• UGIB
– Iced saline gavage and lavage
• Epistaxis
– Pinch and bow, nasal pack, cautery
• Eyes – suspect CSF leak
• Ears – suspect CSF leak