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:



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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).



MRS

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.



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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, IABPb


Pericardial tamponadec


↓

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


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.



MRS

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



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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:



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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 poisoninga


Atropine and other anticholinergicsb


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 antidepressantsa


Amitriptyline, clomipramine, desipramine, imipramine


Older generation antihistaminesa


Diphenhydramine, hydroxyzine (used for itching), chlorpheniramine


Antipsychoticsa


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.

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Dec 11, 2021 | Posted by in EMERGENCY MEDICINE | Comments Off on 14 Emergency Medicine

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