14 Emergency Medicine

“Before running the code, check your own pulse”

– Dr Paul L. Bernstein, Rochester, NY

14.1 Basic Life Support

When a person is found unresponsive:

^aIn patients found unresponsive with suspected spine/head trauma, first step is to stabilize the neck and then only follow the algorithm given below (head tilting is contraindicated in this case).

^bThis scenario can have multiple causes, but one common cause is an arrhythmia. Nowadays, automated external defibrillators (AEDs) are widely available (e.g., shopping malls) and can be life-saving.

Abbreviation: AED, automated external defibrillator.

MRS

When found unresponsive check call CAB:

Check unresponsiveness
Call 911
Address circulation, airway, and breathing

Circulation and airway are very important

When you see “IV fluids” among answer choices in any question, immediately look at the blood pressure and heart rate. If BP is low (SBP ≤ 90), heart rate is >90/min and/or there are other features of volume depletion (e.g., dry oral mucosa, orthostatic drop in BP), then IV fluid resuscitation is always the right answer.

¹ Fluids most commonly used for resuscitation are normal saline and lactated ringers. In profoundly acidotic patient (blood pH ≤ 7), IV bicarbonate is preferred for volume resuscitation.
Similarly, apply this strategy when an exam-question has “intubation” as an answer choice. Look at the respiratory rate, arterial blood gas, etc.

14.1.1 Initial Empiric Treatment in Altered Mental Status

² This is typically done by emergency medical technicians outside of hospital.

Dextrose	For possible hypoglycemia (if blood glucose testing is not available)
Naloxone	Given to patients with signs of opiate poisoning (look for low respiratory rate)
Thiamine	IV dextrose can precipitate acute thiamine deficiency (due to increased consumption of thiamine). This is more likely to occur in patients with low thiamine levels (e.g., alcoholism, severe malnutrition).

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DeNT

14.2 Wernicke-Korsakoff Syndrome

Background	Typically occurs in alcoholics or severely malnourished patients, due to thiamine deficiency. Can be precipitated by administration of IV glucose without thiamine.
Presentation	Wernicke’s syndrome or encephalopathy	Delirium (confusion). Oculomotor dysfunction: nystagmus, lateral rectus palsy (almost always bilateral), and conjugate gaze palsy (due to involvement of oculomotor nerve). Gait ataxia. Imaging may reveal small lesions in midline brain structures.
	Korsakoff syndrome	After acute features of Wernicke improve, patients may develop chronic memory impairment. Presentation: Retro-anterograde amnesia, apathy of amnesia, and confabulation (patient typically makes up for what they cannot remember: an “honest” lie). Common imaging finding is atrophy of mammillary bodies.
Management	Thiamine replacement. Supportive treatment.

MRS

WERNICKE’S DOG

14.3 Causes of Circulatory Collapse

For pulseless ventricular tachycardia or v-fib, please refer to Chapter 4, cardiology for further details

Pulseless electrical activity

14.3.1 Pulseless Electrical Activity (PEA)

Definition: Electrocardiography (EKG) or telemetry shows electrical activity, but patient does not have a pulse.

Etiology:

4H		4T
Hypovolemia	NSIM volume resuscitation ^a	Toxins	For example, overdose with sedatives, tricyclic antidepressants, heroine, etc.
Hyperkalemia or Hypokalemia	Hyperkalemia is common in dialysis patients who have missed treatment.	Tamponade (cardiac)	NSIM: pericardiocentesis
Hypoxia	For example, PEA arrest due to hypoxia can occur in patients with acute aspiration event.	Thrombosis (in pulmonary or cardiac vasculature)	For example. large pulmonary embolus or severe heart attack.
High acid (acidosis)	Missed dialysis treatment is a double trouble: acidosis and hyperkalemia.	Tension pneumothorax	NSIM: bedside needle thoracocentesis
^a To address severe hypovolemia (e.g., in an ongoing bleeding), adequate IV access is necessary (at least two large-bore peripheral IV lines, or a central venous catheter/introducer ³ Introducer is a large bore central-venous catheter. needs to be placed ASAP).
Abbreviation: TCA, tricyclic antidepressant.

14.4 Shock

Clinical Case Scenarios

You have just admitted a patient with profound hypotension to ICU. Invasive hemodynamic monitoring is established. The cause of shock needs to be identified.

^aThere is compensatory increase in SVR/TPR (alpha-1 mediated vasoconstriction) in an effort to maintain BP and tissue perfusion. Legend: “→” = leads to

^bIn early septic shock, inflammatory cytokines lead to primary vasodilation (low TPR/SVR) and compensatory increase in cardiac output (increased cardiac index) → increased blood flow and velocity → decreased oxygen extraction by tissues → normal or high Mean Venous Oxygen content.

^cIn neurogenic shock (e.g., cervical or high thoracic spinal cord injury), there is sudden loss of sympathetic stimulation, which leads to primary vasodilation and a decrease in preload and cardiac contractility → low cardiac output → decreased velocity of blood flow → increased extraction of oxygen by tissues → low MVO₂.

^dIn late septic shock the heart starts failing (with development of decreased cardiac output, increased PCWP, and low MVO₂).

Abbreviations: MVO₂ content, mean venous oxygen content; NSIDx, next step in diagnosis; PCWP, pulmonary capillary wedge pressure (which is an indirect measurement of left heart pressure); SVR/ TPR, systemic vascular resistance (a.k.a. total peripheral resistance).

14.4.1 Hemodynamic Parameters in Different Causes of Shock

	Cardiac output (cardiac index) and MVO₂	PCWP	SVR/TPR	Management
Hypovolemic shock	↓	↓, or N	Increased	IV fluid resuscitation
Right ventricular failure ^a	↓	↓	Increased	IV fluid ± dobutamine
Left ventricular failure	↓	Increased	Increased	Inotropic vasopressors (dobutamine, dopamine) and if refractory, IABP^b
Pericardial tamponade^c	↓	Increased	Increased	Pericardiocentesis
Anaphylactic shock	Increased	↓, or N	↓	IV fluids + epinephrine + antihistamines + IV steroids
Early septic shock (hyperdynamic stage of sepsis)	Increased	↓	↓	IV fluids, antibiotics, and vasopressors
Late septic shock	↓	Increased, or N	↓^d	IV fluids, antibiotics, and vasopressors
Neurogenic shock ^MRS-1	↓	↓	↓	Vasopressors like norepinephrine
^aClues to dx are elevated right atrial and right ventricular pressures with low PCWP.
^bIABP = intra-aortic balloon pump. IABP is timed to inflate during diastole to augment coronary perfusion (primary mechanism of action) and deflate during systole, which increases the forward flow by creating a vacuum effect. IABP is contraindicated in patients with severe acute aortic regurgitation.
^cIn pericardial tamponade, look for equalization of pressures in the right and left sides of the heart.
^dSVR/TPR will differentiate cardiogenic shock from late septic shock.
Abbreviations: IABP, intra-aortic balloon pump; MVO₂, mean venous oxygen; N, normal; PCWP, pulmonary capillary wedge pressure; SVR/TPR, systemic vascular resistance.

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^MRS-1 In neurogenic shock, all systems are down.

Clinical Case Scenarios

Patient is in shock and is admitted to ICU. Pulmonary catheterization reveals the following pressure (in mmHg). What is the dx in each case?

⁴ Trick is to look at diastolic pressures only.

Right atrial pressure (normal is 2-6)^a	RV pressure (normal is <25/8)^a	PCWP (normal is <12-15)^b	Diagnosis
18	25/18	18	Pericardial tamponade (there is equalization of pressure in all cardiac chambers)
25	30/20	8	Right ventricular infarction (cardiogenic shock with low PCWP but high right-sided heart pressures)
16	26/14	23	LV failure (cardiogenic shock)
^aDo not memorize these values. They will be provided on exam.
^bPCWP is an important number to know. Would recommend to memorize this value.

14.5 General Management of Poisoning or Acute Drug Overdose

^aLook for oral burns, heavy drooling of saliva, odynophagia, or inability to eat. Patients might also complain of retrosternal and epigastric pain.

^bEGD is contraindicated in patients with suspected perforation or with severe upper airway edema.

^cActivated charcoal is not effective for the following:

Heavy metals: Iron, lead, mercury, arsenic, etc.

Inorganic ions: Cyanide, lithium, fluoride, etc.

Caustics (acid or alkali).

Any form of alcohol ingestion.

^dThe more hours have passed the less the benefits of activated charcoal. It is not effective in situations where absorption is considered complete. This depends on what poison, drug, or chemical was ingested.

In acetaminophen overdose, it can be used up until 4 hours after ingestion.

For organophosphates, it is ineffective after 1 hour of ingestion.

Also, use of activated charcoal is contraindicated in patients with altered mental status as there is increased risk of aspiration.

Abbreviations: CAB, circulation, airway, breathing; EGD, esophagogastroduodenoscopy.

Patients with hx of caustic ingestion can present years later with mechanical dysphagia due to formation of peptic stricture related to scar tissue. Also, this scar tissue can predispose to squamous cell carcinoma of esophagus.

Gastric lavage: It includes placement of a large-bore orogastric tube, followed by repeated fluid instillation and aspiration. This is rarely used nowadays because evidence shows limited benefit and potential risk. It can however be performed in instances when a large amount of toxin has been known to be ingested within 1 hour.

14.6 Identification of Poison or Drug Overdose

Sometimes the cause of poisoning or ingested substance is unknown. Identifying the drug/poison responsible for presentation is very important.

Pupil size can be an important clue:

^aWithdrawal from most sedative drugs results in sympathetic hyperactivity (dilated pupils, hypertension, tachycardia, and wet and clammy skin).

14.7 Cholinergic and Anticholinergic Poisoning

	Cholinergic poisoning (muscarinic agonists)	Anticholinergic poisoning (muscarinic blockers)
Confusion/seizures/ coma	May be present	Present
Skin (sweat glands)	Diaphoretic (clammy)	Dry Impaired heat-loss mechanism may lead to hyperthermia
Urine/bowel	Incontinence (wet) Diarrhea (watery)	Urinary retention Constipation
Pupils	Constricted ≤ 2 mm	Dilated > 5 mm
Drugs	Organophosphate or carbamate poisoning^a	Atropine and other anticholinergics^b
Antidote	Give atropine, if there is evidence of bronchoconstriction or increased respiratory secretions. 2-PAM (PrAlidoxiMe) is an antidote for organophosphate or carbamate poisoning. It acts slowly.	Physostigmine is used for significant symptoms. Benzodiazepine is indicated for agitation and seizures.
^a Organophosphates and carbamates are found in chemical pesticides and work by inhibiting acetylcholinesterase enzyme. Organophosphates = malathion, parathion, etc. Carbamates = methomyl, carbofuran, etc. For treatment of poisoning, avoid further exposure by removing the clothes and washing the body thoroughly. If ingested, administer activated charcoal within 1 hour. Give pralidoxime, if evidence of cholinergic toxicity.
^b Other anticholinergics (muscarinic receptor blockers) are discussed below.

MRS

M-agonist = pro-M = M causes more Miosis and more water (sweating, diarrhea, and vomiting). Opposite to this, M-blockers cause dryness and pupillary dilation.

Other MRS is: “You should not block Me. If you block Me, I will be: mad as a hatter

dry as a bone
red as a beet
hot as a hare

The following drugs and chemicals can present with symptoms of anticholinergic (atropine-like) poisoning:

Most have sedating properties and can cause confusion, seizures, and coma	Drugs
Tricyclic antidepressants^a	Amitriptyline, clomipramine, desipramine, imipramine
Older generation antihistamines^a	Diphenhydramine, hydroxyzine (used for itching), chlorpheniramine
Antipsychotics^a	Chlorpromazine, thioridazine
Antispasmodics	Dicyclomine (used for irritable bowel syndrome) Oxybutynin (used for bladder hyperactivity) Cyclobenzaprine (a.k.a. flexeril) used for muscle spasms
Anti-parkinsonian drugs	Benztropine, trihexyphenidyl
Hallucinogenic plants	Jimson weed, deadly nightshade (Atropa belladonna), angel’s trumpet, etc.
^aThey also have alpha-blocking properties and can cause hypotension.