I n t e r n a l M e d i c i n e

Summary of

Medical
Emergencies
1- Endocrine Emergencies …………………………. 1
2- DKA …………………………………………….…….……………….. 4
3- Potassium Disorders ………….…………………… 7
4- UGIB …………………………………………….……………..……… 9
5- Emergencies in Liver Cirrhosis .……….. 11
6- ACS ……………………………………………..……………………. 12
7- Cardiac Dysrhythmias ……………….………… 14
8- Hypertensive Encephalopathy .……… 16
9- DIC ……………………………………………...……………….…….. 18
10- Acute Asthma Exacerbation ………….. 20
11- Acute Exacerbation of COPD ……..... 22
12- Pulmonary Edema ………………………………….. 23
 1- Endocrine Emergencies

Adrenal crisis:
 This is a potentially fatal condition associated mainly with an acute deficiency
of the glucocorticoid cortisol and, to a lesser extent, the mineralocorticoid
aldosterone, in a patient with chronic adrenal insufficiency.

Precipitators:
 Major or minor  Burns  Hypermetabolic
infections  Pregnancy states
 Injury  General
 Surgery anesthesia
 The most common cause of adrenal insufficiency is ACTH deficiency
(secondary adrenocortical failure), usually because of inappropriate
withdrawal of chronic glucocorticoid therapy or a pituitary tumor. Congenital
adrenal hyperplasias and Addison's disease (primary adrenocortical failure)
are rare.
 Other causes include tuberculosis, HIV, Bilateral adrenal gland hemorrhage in
sepsis or coagulopathy.

Presentation:
 hypotension  Anorexia,  Hypercalcemia
 Weakness, malaise nausea, vomiting  Weight loss
and fatigue and severe  Hyperpigmentati
 Shock abdominal pain on if excess
 fever  Hypoglycemia ACTH
 Hyponatremia
Management
 Correct volume depletion , I.V. saline as required to normalize BP and pulse
 Replace glucocorticoids I.V hydrocortisone succinate 100 mg stat
 Continue parenteral hydrocortisone (50-100 mg I.M. 6-hourly) until the
patient is well enough for reliable oral therapy. Fludrocortisone may be
considered.
 Correct other metabolic abnormalities, hyponatremia, hypoglycemia,
hyperkalemia
 Identify and treat underlying cause, consider acute precipitant, e.g. infection
 When patient is stable, give the daily replacement dose of cortisol.

1
Myxedema Coma:
 Myxedema coma is a loss of brain function, and decreased level of
consciousness as a result of severe, longstanding low level of thyroid hormone
in the blood (uncontrolled hypothyroidism). It is a medical emergency.
 Seen more frequently in elderly patients and in women, and patient appears
myxedematous (puffy, apathetic), and mainly in winter.
 Hypoglycemia, infection and cold exposure may precipitate myxedema coma.

Presentation:
1) Confusion 6) Hyponatremia
2) Coma 7) Convulsion
3) Hypothermia (body 8) ADD symptoms of
temperature may be as low as hypothyroidism (cold
25°C) intolerance, weight gain, dry
4) Hypoventilation skin, constipation)
5) Cardiac failure 9) hypoglycemia
 Mortality may reach 50%, depends on early recognition and treatment
 Treatment should begin immediately with suspicion.
 Treatment: an intravenous injection of 20 μg triiodothyronine (T3) followed by
further injections of 20 μg 8-hourly until there is sustained clinical
improvement.
 OR An intravenous loading dose of 500-800 mcg of levothyroxine is followed
by a daily intravenous dose of 50-100 mcg
 In survivors there is a rise in body temperature within 24 hours and, after 48-
72 hours, it is usually possible to switch patients on to oral thyroxine in a dose
of 50 μg daily.
 Slow rewarming for hypothermia.
 Cautious use of intravenous fluids to correct hypoglycemia and hyponatremia
(preferably glucose saline), broad-spectrum antibiotics and high-flow oxygen.
 Mechanical ventilation if necessary.
 Hydrocortisone 100 mg IV q8 hrs (bcoz of possible hypothyroidism due to
hypopituitarism).

2
Thyrotoxic crisis: (thyroid storm)
 This is a rare but life-threatening complication of thyrotoxicosis.
 Thyrotoxic crisis is most commonly precipitated by stress, infection in a
patient with previously unrecognised or inadequately treated thyrotoxicosis.
 It may also develop shortly after subtotal thyroidectomy in an ill-prepared
patient or within a few days of 131I therapy when acute irradiation damage
may lead to a transient rise in serum thyroid hormone levels.
 It is a medical emergency, which has a mortality of 10% despite early
recognition and treatment.

Presentation: (Increase in hyperthyroidism symptoms)

1. Fever (hyperpyrexia) 6. Eventually delirium, coma and
2. Agitation (restlessness) death
3. Confusion 7. Other hyperthyroidism
4. tachycardia or atrial fibrillation symptoms like heat intolerance,
5. cardiac failure in the older tremor, sweating, flushing
patient.

Management:
 Patients should be rehydrated (dextrose solution) and given oxygen.
 Broad-spectrum antibiotic is given
 Propranolol, either orally (80 mg 6-hourly) or intravenously (1-5 mg 6-hourly).
 Oral carbimazole 40-60 mg daily should be given to inhibit the synthesis of
new thyroid hormone. OR propylthiouracil (PTU) 200 mg q4 hrs (which inhibits
thyroid hormone synthesis and peripheral conversion of T4-T3)
 Dexamethasone (2 mg 6-hourly) or hydroxortisone IV 100 mg 6-hourly have
similar effects. (also inhibits peripheral conversion)
 Sodium ipodate or potassium iodide (Lugol's solution)
 Applying ice packs and cooling blankets and by administering acetaminophen
(15 mg/kg orally or rectally every 4 h).

Done By Ahmad Shyoukh

3
 2- Diabetic Ketoacidosis
It is the most common endocrine emergency seen by primary physicians mainly in
patients with type 1 DM.
DKA can be the first presentation of type 1 DM in about 25% of patients. Simply,
most of the patients reduce their insulin doses under acute illnesses in the belief that
less insulin is required in these situations.
DKA is a triad of hyperglycemia, hyperketonemia and metabolic acidosis.
Hyperglycemia will lead to osmotic diuresis causing fluid and electrolyte loss (mainly
Na and K).
So patients are severely dehydrated (avg fluid loss about 6L), plasma level of K is
increased but the total body K is decreased, Na level will be decreased.
Insulin deficiency accompanied by increased counter regulatory hormones causes
increased lipolysis and free fatty acids so increased ketosis (ketogenesis exceeds
hepatic capacity to metabolise acidic ketones).

Clinical picture:
DKA can be precipitated by any stressful condition causing increase in counter
regulatory hormones. infection is the commonest precipitant, dehydration, trauma,
MI, surgery … etc.
Clinically the patients presents with sever polyuria, polydipsia, nausea and vomiting,
abdominal pain (could be confused with acute surgical abdomen), blurred vision.
On examination, signs of dehydration would be apparent, hypotension, tachycardia,
kussmaul breathing (rapid and deep breathing as a compensation for acidosis),
acetone breath, hypothermia (so no fever in case of infection), and alteration in LOC
(coma in 5% only).

Investigations:
- Serum glucose <= 250 mg/dl
- Elevated BUN (due to renal hypoperfusion), reduced HCO3 level ( >15 mmol/L)
- Serum Electrolytes
- Arterial blood gases
- Urinalysis for ketones
- ECG and cardiac enzymes
- Infection screen (CBC, blood and urine cultures, chest X ray .. etc)
Management:
1) Fluid replacement with 0.9% NaCl

4
 1L over 30 min >>> 1L over 1h >>> 1L over 2h >>> 1L over 4h
When serum glucose falls to > 15 mmol/l (270 mg/dl) switch to 5% dextrose.
2) Glucose control using Insulin (Low-dose insulin regimen)
Try to avoid the SC route because of decreased absorption (due to dehydration)
so we mainly use IV infusion pump or IM route.
6U/h initially
3U/h when glucose > 270 mg/dl
2U/h when glucose > 180 mg/dl
If no improvement in level of glucose within 1h we should increase the dose of
insulin till the desired level is achieved.
The rate of reduction of glucose level should not exceed 55-110 mg/dl/h to avoid
hypoglycaemia and cerebral oedema.
3) Potassium replacement should be started with insulin.
20 mmol/h KCl when K > 3.5 mmol/l
10 mmol/h KCl when k = 3.5 – 5 mmol/l
Always check the rhythm of your patient.
- Bicarbonate should only be given when sever acidosis (PH > 7).
- Consider using antibiotic only when infection is likely.

Complications of DKA:
1) Cerebral oedema (the commonest cause of DKA mortality in children)
Due to aggressive treatment with hypotonic solution or using HCO3 or rapid
reduction of glucose.
It’s diagnosed by MRI treated by mannitol or hypertonic saline.
2) MI, DIC, thromboembolism, circulatory failure.
3) Acute respiratory distress syndrome.
4) Fluid overload.

Prognosis:
Overall mortality rate is 2%. Deep coma, hypothermia, oliguria, old age, other
comorbidities are signs of poor prognosis.

Hyperosmolar Hyperglycemic Nonketotic Coma (HHNC)

It’s an acute complication more common in type 2 DM characterized by:
- Serum glucose < 600 mg/dl or even higher
- Elevated serum osmolality < 320 mOsm/kg
- PH < 7.3 (no acidosis)
- Dehydration up to 9L
- Mild ketonuria, no ketonemia

5
 Clinical picture:
It is the initial presentation of type 2 DM in 30-40% of patients. Symptoms and signs
are the same of those in DKA with some differences:
- Abdominal pain is much commoner in DKA
- Coma is more common in HHNC (especially when serum osmolality < 340
mOsm/kg)
- Focal neurological deficits is more common in HHNC (lethargy, coma, seizures,
sensory deficits, hemiparesis … etc)

Management:
Airway management is the top priority
Rapid and aggressive volume replacement is indicated using isotonic NaCl
(1-2L of 0.9% isotonic saline over the first hour after 0.5L bolus dose) but you have to
be careful in patients with cardiac or renal failure, in elderly and in children.
Half the dose of insulin used in DKA is used here (3U/h) (in HHNC, patients are
relatively insulin sensitive
Potassium may be added to the infusion fluid and should be started at a level of 5
mEq/L or less. Mortality is higher (40%) than in DKA.

Hypoglycaemia
a reduction in plasma glucose concentration to a level that may induce symptoms or
signs (usually less than 3.5 mmol/l or 63mg/dl).
It is usually caused by insulin overdosing in type 1 DM or sulphonylurea in type 2 DM.
- Symptoms of autonomic nervous system activation: Sweating, trembling,
tachycardia, hunger and anxiety.
- Neuroglycopenic symptoms: confusion, drowsiness, speech difficulty,
incoordination, irritability.
Causes are insulin overdosing, heavy exercise, alcohol, poor diet … etc
Treatment is by oral carbohydrate for mild cases.

6
 3- Potassium Disorders
 Normal plasma level of K: 3.5 – 5 mEq/L " major intracellular cation (95-98%)"
 Kidneys excrete 90% of the daily intake of K, while only 10% is lost through GIT.
 Causes of hypokalemia:
 Decreased intake : intake of < 25 mmol/day.
 Gastrointestinal losses: vomiting, diarrhea, tube drainage and laxative abuse.
 Shift into cells: metabolic alkalosis, increased insulin, beta adrenergic activity, the
replacement of vitamin B12 in B12-defiecnt patients and theophylline.
 Urinary losses:
1- Diuretics, mineralocorticoids and high-dose glucocorticoids
2- increased aldosterone states: Conn syndrome, excessive licorice ingestion, bartter syndrome (genetic
disease causing salt loss in loop of Henle), Gitelman's syndrome (distal convoluted tubule
dysfunction >> thiazide-like effect), cushing disease.
3- hypomagnesemia: there are magnesium-dependent potassium channels. When magnesium is low,
they open and spill potassium into the urine.
4- renal tubular acidosis type I and II.
 Others: Pseudohypokalemia, Some antibiotics like penicillins and aminoglycosides,
Hypokalemic periodic paralysis.
 Hypokalemia manifests as disturbances in the function of excitable tissues:
 Skeletal muscles: weakness particularly of the lower extremities, fatigue, rhabdomyolysis,
muscle cramps, even paralysis may ensue.
 Smooth muscles: GI ileus, nausea, vomiting.
 Cardiac muscles: prominent U wave on EKG, cardiac arrest, enhanced digitalis toxicity.
 Peripheral nerves: decreased or absent tendon reflexes.
 Polyuria, polydepsia: Potassium is necessary for ADH effect on the kidney, patients may
present with nephrogenic diabetes insipidus.
 In emergency cases, the most important diagnostic test is EKG.
 Measurement of plasma electrolytes, bicarbonate, urine potassium and sometimes of plasma calcium
and magnesium is usually sufficient to establish the diagnosis.
 EKG changes: U waves (the most characteristic finding), others: ventricular ectopy (PVCs), Broad
flat T waves, ST depression, and QT prolongation.
 Treatment:
o Correction of underlying cause when possible.
o Repletion:
Oral KCL supplement:the safest method. there is no maximum rate of oral K replacement.
Hypokalemia is refractory to correction in the presence of Magnesium deficiency.
If hypokalemia is severe (<2.5 mmol/L) and/or oral supplement is not tolerated or the patient has
arrhythmia secondary to hypokalemia, IV KCl (maximum 10–20 mEq/hr) can be administered
through a central line with cardiac monitoring in ICU, at rates that should not exceed 20 mmol/hr in
case of central line, or 10 mmol/hr in peripheral line.
Do not use dextrose containing fluids, they increase insulin release and lower potassium.
KCl should always be given in saline solution.
Potential complication of too rapid repletion is fatal arrhythmia >> Must be very slow.
Hyperkalemia:
 Causes of hyperkalemia:
o Pseudohyperkalemia "falsely elevated levels": Hemolysis, Repeated fist clenching with tourniquet
in place, Thrombocytosis or leukocytosis will leak out of cells in the lab specimen.

7
o Decreased excretion: Renal failure
o Decreased aldosterone:
 ACE inhibitors/ARBs
 Type IV renal tubular acidosis (hyporeninemic hypoaldosteronism)
 Spironolactone and eplerenone (aldosterone inhibitors).
 Triamterene and amiloride (potassium-sparing diuretics)
 Trimethoprim.
 Addison disease.
o Release of potassium from tissues:
 Any tissue destruction, such as hemolysis, rhabdomyolysis, burns or tumor lysis syndrome.
 Decreased insulin.
 Acidosis: cells will pick up hydrogen ions and release potassium in exchange.
 Beta blockers and digoxin.
 Heparin.
 NSAIDs.
 Clinical features:
o Weakness, begins when level > 6.5
o Paralysis when severe.
o Ileus (paralyzes gut muscles), Nausea, vomiting,
intestinal colic, diarrhea.
o Cardiac rhythm disorders. Ventricular fibrillation,
palpitations, Sudden death from asystolic cardiac
arrest.
o Decreased deep tendon reflexes, Paresthesia.
o Respiratory failure.
Sometimes there are no symptoms until cardiac arrest occur.
Hyperkalemia does not cause seizures
 Treatment of hyperkalemia:
Life-threatening hyperkalemia (abnormal EKG and/or K ≥ 6):
o Calcium chloride or calcium gluconate IV. Through a central line or a large cannula in a big vein to
avoid delay. the difference between calcium chloride and calcium gluconate: calcium chloride
contains more calcium and is typically reserved for use in codes (increased risk of tissue necrosis).
Calcium stabilizes the resting membrane potential of myocardial membrane >> decreases
membrane excitability, use it in caution in patients on digitalis because hypercalcemia predispose to
digitalis toxicity.
 Calcium does not lower the potassium level.
Shift potassium into cells:
 Glucose and Insulin : give both to prevent hypoglycemia.
 Bicarbonate.
 Inhaled beta agonists: nebulaized salbutamol.
Removing potassium from the body:
 Cation-exchange resin like Sodium Polystyrene "kayexalate" or calcium resonium: removes
potassium from the body through the bowel, given orally or rectally. Exchange K for Na or Ca in
the gut. Given in sorbitol to prevent constipation.
 Loop diuretics
 hemodialysis or peritoneal dialysis: most rapid and effective way of lowering plasma K.
reserved for intractable hyperkalemia and those with renal failure.
Done By: Amna Ibrahim

8
 4- Management of Upper GI Bleeding
Mortality in UGIB depends on:
I. Intravenous access (at least 1 large-bore cannula) 1. Age
II. Fast initial assessment: 2. Shock status
1. Circulation status: look for tachycardia, 3. Co-morbidity
hypotension, oliguria and if the patient cold, 4. Diagnosis of bleeding
sweaty, or agitated. 5. Evidence of bleeding
2. Evidence of liver disease: look for jaundice, during endoscopy
coetaneous stigmata, hepatosplenomegaly or Revise Rockall score in page 853 in
ascitis. Davidson 21st edition

3. Comorbidity: look for cardio-respiratory, cerebrovascular or renal disease.

III. Basic investigations: (you should know why you order each investigation -as the Dr said)
1. Full blood count:
Causes of UGIB
 Anemia in sub-acute or chronic UGIB.
 Normal Hb concentration in major bleeding till 1. Peptic ulcer (50%)
haemodilution occurs. 2. Gastric erosion (20%)
2. Urea and electrolytes: 3. Esophagitis (10%)
 Blood urea and creatinine are high > renal failure. 4. Varices (10 %)
5. Mallory-weiss tear (5%)
 Blood urea is high but creatinine is normal >
6. Vascular malformation
severe bleeding (due to absorption of luminal
(5%)
blood).
7. Cancer of the stomach
3. LFT (for chronic liver disease). or easophagus (2%)
4. Prothrombin time (in 1liver disease or 8. Aorto-duodenal fistula
2
anticoagulated patient). (0.2%)
5. Cross matching (at least two unites).
IV. Resuscitation:
1. Give intravenous crystalloid or colloid fluids if the patient is hypotensive.
2. If he still hypotensive or actively bleeding; transfuse whole blood.
3. If you suspect chronic liver disease, give broad-spectrum antibiotics.
4. With severe bleeding and the presence of cardiac disease, do central venous
pressure.
V. Oxygen:
- For any shocked patient via facemask.
VI. Endoscopy:
 Done after adequate resuscitation, within the first 24 hours.
A- Diagnostic in 80% of cases.

9
 ► If the cause is other than varices:
B- Therapeutic: In patients with major endoscopic stigmata (like visible vesselor
overlying clot) or active bleeding.
1. Inject diluted epinephrine into the bleeding point.
2. Do thermal modality or metallic clip.
3. Give intravenous PPI therapy (reduces rebleeding and the need of surgery
but does not reduce the mortality).
VII. Hourly monitoring: (1pulse, 2blood pressure, 3urine output)
VIII. Surgery:
 Type of the surgery depends on the site and the diagnosis:
1. For duodenal ulcer do under-running with or without pyloroplasty
2. For gastric ulcer do under-running and biopsy must be taken.
3. Local excision.
4. If neither is possible do partial gastrectomy or Indications for surgery
arterial embolization.
1. Failure of therapeutic
 All patients should take H. Pylori eradication and
endoscopy.
avoid NSAIDs if the cause is an ulcer.
2. Rebleeding once in
► If the cause is varices: elderly or frail patient
IX. Therapeutic Endoscopy: 3. Rebleeding twice in
 More urgent endoscopy is indicated if varices are young, fitter patient.
strongly suspected.
1. Banding ligation:
- Repeated every 1-2 weeks until varices are obliterated.
- The most widely used initial treatment, stops variceal bleeding in 80%.
2. Sclerotherapy:
- Associated with more side effects (esophageal perforation / strictures).
► If endoscopy was difficult (due to active bleeding), bleeding should be controlled by:

X. Balloon tamponade (Sengstaken-blakemore tube):

 The tube has four lumens for 1esophageal aspiration, 2esophageal ballooning, 3
gastric aspiration, 4 gastric ballooning.
XI. Pharmacological treatment:
1. Vasopressor (terlipressin): prevent rebleeding, reducing the active bleeding
during the endoscopy.
2. PPIs: Prevent peptic ulcers
XII. Esophageal transaction: used when the bleeding cannot be controlled by other
modalities. It has considerable morbidity and mortality, and now rarely used.
Remember: the overall mortality rate in UGIB is 10% !!

01
 Hepatic Encephalopathy Ascites Spontaneous Bacterial Peritonitis
 Splanchnic vasodilatation (due to

Pathophysiology
mediator mainly nitric oxide) so 11
 Toxin (ammonia) produced in the  Infection from ascitic fluid
decrease in BP so renin- angiotensin
gut, which is normally removed by  Translocation from intestine
system activation so salt and water
healthy liver, bypass liver by porto-  Usually monomicrobial (E.coli
retention.
systemic shunts. being the most common)
 Reduced albumin.
5- Emergencies in a patient with Liver cirrhosis

 Portal hypertension.
 Abdominal distention (appear when 1
L accumulate), flank fullness, shifting
 Decrease consciousness, poor  Fever, abdominal pain,
Presentation

dullness, fluid thrill.

concentration, disorientation, sleep tenderness.
 USS, paracentesis (here in cirrhosis,
disturbances, psychiatric changes,  Unexplained encephalopathy.
the fluid is transudate so total protein
flapping tremor and maybe coma.  Leukocytosis (>250 cells/mm3
concentration <25 g/l, ascites albumin
 High ammonia in blood. diagnostic).
lower than serum albumin by 11 g/l or
more).

 Increase protein load (include GI

Precipitating
factors

bleeding), constipation, infection,

Nothing Nothing
dehydration, drugs (sedatives),
hypokalemia.

 Treat underlying cause.

 lactulose (15-30 Ml 8-hourly orally),
if patient was unconscious give it by
NG tube or rectally.  3rd generation cephalosporins
 Sodium restriction (no added salt diet)
 Neomycin (1-4g 5-hourly). If not (cefotaxime, ceftriaxone) are
Treatment

 Diuretics: spironolactone is the DOC.

available give metronidazole (to agents of choice for treatment.
Patient may need loop diuretics.
reduce bacterial content of the  Ciprofloxacin (250 mg daily) or
 Paracentesis with IV albumin.
bowel). norfloxacin (400 mg daily) as
 TIPS.
 liver transplant. prophylactic.
 Protein restriction is not
recommended (but do not ingest
excess protein).
 A c u t e6-
C o r o n Coronary
Acute d r o me (A C S )
a r y S y n Syndrome

Myocardial ischemia typically due to atherosclerotic CK-MB goes back to normal within 48 hours
plaque rupture  coronary thrombosis (used to detect re-infarction).
Troponins need 14 days to normalize.
Remember Other causes of myocardial ischemia: Troponin levels are higher in renal failure.
Spasm: Prinzmetal’s angina, cocaine abuse
Localization of STEMI
Embolus: Atrial myxoma, mural thrombus
Anatomy ECG leads Coronary
Vasculitis: Kawasaki, Takayasu arteritis, SLE, PAN
with STE
Hypercoagulable states: PRV, Factor V Leyden,
Septal V1-V2 LAD
antiphospholipid antibody syndrome
Anterior V3-V4 LAD
Clinical manifestations Apical V5-V6 LAD
Typical Angina: Retrosternal Lateral I, aVL, V5-6 LCx or LAD
pain/tightness/pressure, radiation to neck, jaw, arms, Inferior II, III, aVF RCA
precipitated by exertion, relieved by rest or Right V V1-V2, V4R RCA
nitroglycerin Posterior ST RCA or LCx
in ACS: new-onset, crescendo or at rest depression
Associated Sx: dyspnea, diaphoresis, nausea and in V1-V2
vomiting, palpitations, lightheadedness
May be silent (elderly, diabetics)
UA/NSTEMI
Examination findings Only distinguished by cardiac biomarkers.
Signs of ischemia: S4, new murmur, paradoxical S2 Initial management is the same.
Signs of HF:  JVP, basal crackles, S3, BP, cool These patients may progress to STEMI, so we
extremities have to do risk stratification.
Signs of atherosclerosis: Carotid or femoral bruit,
absent distal pulses  High risk features:
Repetitive or prolonged chest pain
Spectrum of ACS Elevated cardiac markers
Dx UA NSTEMI STEMI Persistent ST depression ≥ 0.5 mm
Coronary Subtotal Total Features of HF: BP, syncope, LVEF <40%
thrombosis Past Hx: DM, CKD, previous CABG or PTCA
History New pain, worse Angina at TIMI risk score (TRS)
pain, rest pain, rest, Age ≥ 65 1
usually < 30mn usually ≥ 3 risk factors for CAD 1
>30 + Known CAD (stenosis ≥50%) 1
associated ASA use in the past seven days 1
sx Severe angina (≥2 episodes of chest 1
ECG ± ST depression STE or pain in the last 24 hours)
and/or TWI new LBBB ST deviation ≥ 0.5 mm 1
Troponin/ - + ++ Positive cardiac markers 1
CK-MB Higher score means higher risk
Higher risk patients (TRS ≥3) benefit more
Cardiac biomarkers from LMWH, GP IIb/IIIa inhibitors and early
TnI, TnT , CK-MB start to rise within 4-6 hours. angiography.

12
Initial management of ACS Remember Streptokinase is allergenic and
The specific indications and benefits of the drugs mentioned should not be repeated within 12 months of
below may differ in pts with UA/NSTEMI vs. STEMI. Refer to administration.
books for more details.
A. Antiplatelets
Fibrinolysis vs. PCI
1. Aspirin: 325 mg chewed/crushed
If the hospital has PCI, it’s superior to
2. Clopidogrel: should be d/c 5 days prior to CABG
fibrinolysis within 90 minutes of arrival (door-
3. Glycoprotein inhibitors: Abciximab/ tirofiban/
needle time)
eptifibatide
If no PCI available, assess time of
presentation, time for transfer, risk of STEMI,
B. Anticoagulants
risk of bleeding to decide what to do, but in
Heparin (UFH or LMWH) until PCI
general, “give thrombolysis then transfer” is
If UFH, titrate PTT to 1.5-2x of control
better than “just transfer”.
C. Adjuvant therapy
Morality rates are improved by
1. Oxygen( keep O2 Sat >90%)
1. PCI
2. Morphine (analgesia, decreases anxiety, for
2. Thrombolysis in STEMI
pulmonary edema)
3. ASA
3. Beta Blockers: C/I in bradycardia, hypotension,
4. BB
heart blocks, bronchospasm
5. Heparin
4. Nitrates: symptomatic relief, no effect on mortality
5. ACEI or ARB: esp. in CHF without hypotension, very
Discharge medications
useful in anterior wall MI
1. ASA: for all patients
6. CCB: for patients who can’t tolerate BB
2. Clopidogrel: esp. if stented
Fibrinolysis 3. BB unless contraindicated
When to use it? 4. Statin (e.g. atorvastatin)
1. STEMI (STE ≥ 1 mm in ≥ 2 leads or new LBBB) 5. ACEI for CHF
2. Within 12 hours of symptom onset 6. Nitrates
3. No contraindications 7. Warfarin only if anticoagulation indicated

Contraindications to thrombolytic therapy Secondary prevention

Absolute Relative Control HTN, DM, Hyperlipidemia, weight loss,
Any prior ICH Severe HTN ≥ 180/110 exercise, stop smoking
Intracranial neoplasm, Trauma or major
aneurysm, AVM surgery within 3 weeks
prior
Nonhemorrhagic stroke Ischemic stroke > 3
The End
or closed head trauma months prior
By: Khaled Shunnar
within 3 months
Active internal bleeding Recent internal
or bleeding tendency bleeding (2-4 weeks),
active PUD
Suspected aortic Pregnancy
dissection

13
 A summery of EMERGENCIES
7- Emergent OF CARDIAC
Cardiac DYSRHYTHMIAS
Dysrhythmias
A) Bradycardia:
 Could be normal, or indicating sinus problem (Sinus Bradycardia) or
atrioventricular block.
 And those could be secondary to medication overdose (e.g. BB, CCB) or sinus
disease like fibrosis or excessive vagal tone or recent MI or simply of infectious
etiology.
1- Sinus Bradycardia: HR < 60 b/min.
2- First-degree AV block: Fixed prolongation of PR interval at a rate of 70 b/min with
no dropped beat.
3- Mobits-type 1 Second-degree AV block: Progressive prolongation of PR interval
until P-wave is blocked and a ventricular beat is dropped.
4- Mobits-type 2 Second-degree AV block: A sudden blocked beat. PR interval
prolongation is not necessarily.
 Management: #1, # 2 and #3 often need no treatment. If necessary they are
treated as #4, with atropine and then pacemaker.
B) Atrial Dysrhythmias:
 Always pathological, with narrow or normal QRS and absence of a normal P wave.
 Well known causes are: Caffeine, Hypotension, Anxiety, Hyperthyroidism,
Alcohol, COPD , PE, Mitral valve disease. (The last 5 causes are mainly for Atrial
Flutter). Atrial Fibrillation is mostly caused by underlying heart disease.
1- Sinus Tachycardia: HR>100 b/min.
2- Paroxysmal SVT: Sudden onset and termination with premature beat. Regular
rhythm with 130-220 b/min.
3- Atrial Flutter: Characteristic sawtooth appearance on ECG.
4- Atrial Fibrillation: Uncoordinated atrial activation with (irregularly, irregular)
rapid ventricular response.
 Management: #1 BB or nothing. #2 start with carotid sinus massage then give
Adenosine. #3 give digitalis, BB, CCB and cardioversion if unstable.
>> For #4 we follow rate control or both rate and rhythm control. (With
anticoagulants).
 As a general role, rate control is enough for asymptomatic patients or with little
symptoms.

14
  Patients having symptoms of arrhythmias or heart failure should receive rhythm
control as well.
- Rate control: CCB, BB given in rest or exercise. Digoxin is given only at rest and for
patients with systolic heart failure.
- Rhythm control: It is either electrical or pharmacological (Amiodarone)
cardioversion.
- Anticoagulants: for practical speaking they are given for all patients to reduce
mortality and morbidity related to stroke, refer to CHADS score in the internet for
more information.
C) Ventricular arrhythmias:
1- Ventricular Tachycardia: No P wave with organized wide QRS complex on ECG.
 Most common etiologies: MI and anatomic cardiac diseases, hypokalemia,
hypomagnesaemia, hypoxia, hypercalcimia, Lithium, Phenothiazines, TCA and
Quinidine.
 Treatment: If stable Amiodarone or Lidocane if not resolved give
procainamide if still then cardioversion. If unstable do electrical cardioversion.
For Torsade de Pointes variant consider BB and also cardioversion if unstable.
2- Ventricular Fibrillation: No signs of organized pattern on ECG. Clinically he/she is
a dead person with a clue of diagnosis on ECG.
 Treatment: For Ventricular Fibrillation I suggest to read it from a good source
(Page 316 in Kaplan 2011 edition is more than enough). Roughly speaking for
these patients you are dealing with immediate CPR and epinephrine injection.
D) Asystole: Clinically a pulseless dead person with Asystole on ECG.
 Treatment: Transcutaneous pacing is considered only for very slow bradycardia.
But not for Asystole. Then administer 1 mg epinephrine IV and push every 3 to 5
minutes.
Note: - Atropine is no longer indicated in Asystole. Bicarbonate is useful when the
underlying cause is related to acidosis, TCA or aspirin overdose, hyperkalemia
and DKA.
NOTE: Pulseless electrical activity is another entity. It occurs in a patient with sever
hypotension to the point of losing their pulse in which there is still some type of
electrical activity on ECG and may even be normal or simple tachycardia.
Here you SHOULD know the underlying cause in anyway. It is the key to therapy.
Generally speaking, start with CPR and epinephrine while determining the etiology.

Done by : Zaker Shawabkeh

August 11, 2013 15
 8- Hypertensive
Hypertensive Encephalopathy
encephalopathy

Definition :- It is a reversible neurological dysfunction caused by sudden and sustained severe

elevation of blood pressure ≥180/120 mmHg.

Etiology :- The most common cause of hypertensive encephalopathy is abrupt blood pressure
elevation in a chronically hypertensive patient .
Other clinical situations that cause abrupt elevation in blood pressure are :-

 Chronic renal parenchymal disease

 Acute glomerulonephritis
 Renovascular hypertension
 Withdrawal from hypertensive agents (eg, clonidine)
 Encephalitis, meningitis
 Pheochromocytoma, renin-secreting tumors
 Sympathomimetic agents (eg, cocaine, amphetamines, phencyclidine [PCP], and lysergic acid
diethylamide [LSD])
 Eclampsia and preeclampsia
 Head trauma, cerebral infarction
 Collagen vascular disease
 Autonomic hyperactivity
 Vasculitis

Clinical Presentation

History Physical Examination

o Headache o On ophthalmoscopy : grade IV retinal

o confusion changes including ( papilledema,
o disturbances of consciousness hemorrhage, exudates, and cotton-wool
o visual disturbances spots )
o nausea, and vomiting o Neurologic examination: reveals transient
o seizures & coma and migratory neurologic nonfocal deficits
ranging from nystagmus to weakness and an
o Symptoms resulting altered mental status ranging from confusion
to coma.
o from end-organ damage like :
o Cardiovascular :- S3, elevated neck veins,
 Cardiovascular symptoms of aortic peripheral edema, murmurs, abdominal
dissection, congestive heart failure, pulsations, and diminished pulses
angina, palpitations, irregular heartbeat, o Renal:- Acute renal failure, pulmonary
or dyspnea . edema, and peripheral edema
 Renal hematuria and acute renal failure .
o Pulmonary:- Pulmonary edema, rales, and
wheezes

16
 Work up :- It’s a diagnosis of EXCLUSION…
 Blood Pressure measurement (v.important)
 CBC : to rule out anemia .
 U/A , BUN & creatinine level : for hypertensive nephropathy.
 Urine toxicology screen to help exclude drug-induced hypertensive encephalopathy.
 ECG & Cardiac Enzymes : to rule out MI.
 chest Xray :- for complications of hypertensive encephalopathy, including aspiration due to
altered mentation. Also to evaluate for other conditions, such as acute pulmonary edema and
aortic dissection.
 CT scans ( to exclude CVA or intracranial hemorrhage ).
 MRI( edema of white matter in parieto-occipital regions).

Treatment :-

 The first thing to do is to lower blood pressure within minutes or hours ( note that
Excessively reduced blood pressure may result in cerebral infarction, blindness and cardiac
ischemia ) by one of these drugs :-
1. Diazoxide ( IV ). It normalizes blood pressure within 3-5 min, and the effect lasts 6–18
hours (Furosemide injected simultaneously with diazoxide enhances both the
antihypertensive effect and its duration )
2. Hydralazine (IV or IM ). “similar to diazoxide action “
3. Sodium nitroprusside ( IV ) .
4. Nitroglycerine .
Baseline BP important “ MAP by 25% & DBP to 100-110 “

 The second thing is to give Oral antihypertensive drugs after the patient recovers from the
most severe symptoms, and intravenous injections are no longer necessary.
 In addition to antihypertensive drugs, anticonvulsant drugs, such as phenytoin, may be given
to the patient with seizures. However, typically anti-hypertensive medication is sufficient for
treatment of neurological symptoms.

Done By :- Tasneem Abu Al Fuol

17
 DIC "Death Is9-
Coming!
DIC … :O"
To be suspected In pts with:
Serious underlying dis. +  bleeding +   (PT & PTT) and  platelets count.

DIC = Disseminated Intravascular Coagulation = Consumptive coagulopathy

(pathological activation of coagulation sys.  Thrombosis  end-organs failure) +
(disrupted natural coagulation regulation  Bleeding + microangiopathic Hemolysis).

What are the underlying causes?

1. Infection  Gram-ve Sepsis (most common), viruses, N.meningitidis,
S.pneumonia, malaria.
2. CA  adenocarcinoma, lung, pancreas, stomach, prostate.
** Promyelocytic leukemia M3  classic association.
3. Massive tissue injury  burn, trauma, massive surgery, rhabdomyolysis,
pancreatitis.
4. Obs. Problems  abruption placenta, amniotic fluid embolism, PET.
5. Vascular abnormalities  giant hemangiomas, aortic aneurysm.
6. Others  heatstroke, snakebite, Hemolysis from transfusion rxn, shock, liver
dis., serotonin syndrome.

Presentation?
1. Bleeding from ANY SITE: most pts (mouth, nose, venipuncture sites, hematurea
due to Foley's cath. Insertion, extensive bruising …).
2. Thrombosis (less common).
3. Hemolysis >> may lead to renal failure (RF), jaundice & confusion.
4. It may be insidious & chronic as in case of CA.

Labs & usual findings?

1. Usually  >> platelets count & fibrinogen concentration (also other coagulation
factors espi. V & VIII).
2. Usually  >> PT, aPT T, thrombin time, FDP (Fibrin Degradation Products: D-dimer).
3. Blood film >> fragmentations on RBC's (schistocytes).

Dx? >> ISTH score <<

1) Presence of associated dis.  essential.

81
 2) Platelets   if >100 /  if <100 /  if <50.
3) FDP   if no increase /  moderate increase /  if strong increase.
4) PT   if <3s /  if (3-6) s /  if >6s.
5) Fibrinogen   if >1 g/L /  if <1 g/L.
>> Total score: if 5 or more >> DIC // if less than 5 >> repeat monitoring over 1-2 days.

How to manage?
1. ICU admission (to control acidosis, dehydration, hypoxia, RF …).
2. According to presentation:
- Bleeding >> FFP, Platelets, Cryoprecipitate (not routine/ only if bleeding OR
to cover high-bleeding- risk intervention).
- Thrombosis >> Heparin (controversial! / But in Davidson's: prophylactic heparin should
be given unless C/I, & therapeutic does "un-fractionated heparin" if established
thrombosis, unless C/I).
3. The PRIMARY tt is >> treat the underlying disorder :)
4. Some pts with sepsis- associated DIC benefit from activated protein C
concentrate.
** Generally DON'T treat DIC pts with antifibrinolytics (ex. tranexamic acid)!

General Notes:
- Cryoprecipitate: fibrinogen (at low temperature).
- FFP: factors 1972.
- Normal PT = 10.5-13.5 sec.
- Normal aPTT= 26-36 sec.
- Normal D-dimer = < 200 micro-g/L.
- Normal Fibrinogen = 1.5-4 g/L.

This summary is enough for DIC topic from the following references:
Davidson's, Kaplan's & Dr's Mahmood Ayesh lec.

 By Your Sis.: Ghada Odeh … bettawfee2 ,,, da3watkom :)

81
 10- Acute
AcuteAsthma
Asthma Exacerbation
Exacerbation

PEFR should be recorded immediately in all patients if possible, and management should be
started according to severity of asthma.

Moderate asthma
(Patients with increasing symptoms, PEFR 50-70%, and no features of acute severe asthma)

Treat with high flow oxygen and Nebulized B2-agonist, if they improve and are then stable for at
least 1 hour, discharge with oral prednisolone daily for 1 week.

For long term control of moderate asthma:

Daily inhaled steroids + inhaled B2-agonists as needed.

Severe asthma
(PEFR <50%, with features of acute severe asthma) 1

Initial treatment:
 Oxygen therapy to maintain O2 saturation of 94-98%.
 Nebulized B2-agonist (salbutamol 5mg or terbutaline 10mg).
 Systemic corticosteroids (oral prednisolone 30-60mg or IV hydrocortisone 200mg).
 Antibiotics if evidence of infection on chest X-ray, purulent sputum.
 IV fluids if necessary.
 Investigations. 2

If improved- continue- Poor response, or life-threatening features

 Oxygen therapy.  Oxygen therapy.
 Nebulized B2-agonist 4-hourly.  Nebulized B2-agonist every 10-20
 Oral prednisolone for 1 week. min.
After 24 hours  IV hydrocortisone 4-hourly.
 Add high-dose Inhaled  Nebulized Ipratropium bromide.
corticosteroid.  IV Magnesium sulphate.
 Change to inhaled B2-agonist.
 Discharge.3  Mechanical ventilation if needed.4

For long term control of severe asthma:

Daily inhaled steroids + inhaled B2-agonists as needed + antileukotriene & oral steroids.

20
1 Features of acute severe asthma:
1. Inability to complete a sentence.
2. Pulsus paradoxus.
3. HR > 110/min
4. RR > 25/min
5. PEFR < 50% of expected.

Features of life-threatening asthma:

1. Cannot speak, silent chest, central cyanosis.
2. Exhaustion, altered level of consciousness.
3. Bradycardia or hypotension.
4. PEFR < 33% of predicted.

2 Investigations:

 Chest X-ray to exclude pneumothorax or pneumonia.

 Continuous pulse oximetry.
 ABGs if SpO2 < 92%.
 PEFR every 15-30 minutes to assess early response, and charted before and after
bronchodilator treatments.
 Urea and electrolytes.

3 Discharge when:
 Free of SOB or wheeze.
 PEFR > 75% predicted & diurnal variation <25%
 Stable on discharge treatment for 24 hours.

4 Indications for assisted ventilation:

 Coma.
 Respiratory arrest.
 Deterioration of ABGs despite optimal therapy.
 Exhaustion, confusion, drowsiness.

_____________________________
References: Kumar & Clark’s, Davidson’s, Kaplan.

21
 11- Acute Exacerbation of COPD

Characterized by:
- Increase in symptoms (increase dyspnea, increase volume of sputum,
production of purulent sputum).
- Decrease in lung function / health status.

Causes:
- Viral infection (most common)
- Bacterial infection
- Heart failure
- MI
- PE
- Lung CA
- GERD
- Drugs (B-blocker)

Initial management:
- O2 saturation
- ABG
- CXR
- CBC
- ECG
- Peak Expiratory Flow

Specific management:
- Oxygen (controlled at 24% / 28% | aim SaO2 at >90%)
- Bronchodilators + anticholinergic ( Salbutamol + Ipratropium)
- Corticosteroids = Oral prednisolone (30mg for 10 days)
- Antibiotic (if needed)
- Non-invasive ventilation (eg:BiPAP)
- Additional therapy (if needed. eg: peripheral edema : Diuretics)

22
Medical Emergencies Group B – Heba Abdelnabi
12- Pulmonary
Acute Pulmonary Edema
Edema
Pulmonary edema occurs when fluid leaks from the pulmonary capillary network into the lung interstitium
and alveoli, and the filtration of fluid exceeds the ability of the lymphatics to clear the fluid.

>> Life threatening, acute development of alveolar lung edema is most often due to

(1) Elevation of hydrostatic pressure in the pulmonary capillaries (left heart failure, mitral stenosis).
(2) Increased permeability of the pulmonary alveolar-capillary membrane.

Cardiogenic : Non-cardiogenic :

>> Physical findings :

- Patient looks severely ill, sitting upright (orthopnea),

tachypneic/Dyspneic, cyanosis may be present,

- Pink frothy sputum, bilateral rales/ crakles, third heart sound, raised JVP, pulsus alternans.

>> Lab data : early stage >> low PaO2 and PaCO2, later >> progressive respiratory failure, hypercapnia and
academia

>> CXR : cardiomegaly, pulmonary vascular redistribution, diffuse haziness in lung fields, perihilar butterfly
/bat wings appearance, kerly B lines, small effusions at costophrenic angles.

>> Management : immediate and aggressive :

- Seat pt. upright to reduce venous return.
- Administer 100% O2 by mask to achieve PaO2 >60 mmHg. !! >> less % with lung disease
- IV loop diuretic ( furosemide 40-80 mg ) !! >> lower doses if the pt doesn’t take diuretics chronically.
- Morphine (2-5 mg) IV or Diamorphine (2.5-5 mg) IV. !! >> caution in liver failure and COPD.
- Afterload reduction : If systolic BP > 100 mmHg, start nitrate IV infusion but keep systolic BP >90mHg.
< 100 mmHg, treat as cardiogenic shock, use inotropic agents.
- Treat the underlying cause whether cardigenic or non-cardiogenic and keep monitoring : BP, pulse, RR,
JVP, ABG, urine output, and repeat CXR and ECG.

Harrison’s handbook / Oxford handbook / http://www.patient.co.uk/doctor/acute-pulmonary-oedema

23