Triads in Medicine – Rapid Review for Medical Students

triads in medicine

One of the most convenient ways of learning and remembering the main components of disease and identifying a medical condition on an exam are Triads, and medical students/interns/residents swear by them.

Be it a question during rounds, a multiple-choice exam question to be solved, or even in medical practice, the famous triads help physicians recall important characteristics and clinical features of a disease or treatment in an instant.

Since exam season is here, this could serve as a rapid review to recall the most common medical conditions.

While there are a vast number of triads/pentads available online, I have listed the most important (high-yy) ones that every student would be asked about at least once in the duration of their course.

1) Lethal Triad also known as The Trauma Triad of Death
Hypothermia + Coagulopathy + Metabolic Acidosis

2) Beck’s Triad of Cardiac Tamponade
Muffled heart sounds + Distended neck veins + Hypotension

3) Virchow’s Triad – Venous Thrombosis
Hypercoagulability + stasis + endothelial damage

4) Charcot’s Triad – Ascending Cholangitis
Fever with rigors + Right upper quadrant pain + Jaundice

5) Cushing’s Triad – Raised Intracranial Pressure
Bradycardia + Irregular respiration + Hypertension

6) Triad of Ruptured Abdominal Aortic Aneurysm
Severe Abdominal/Back Pain + Hypotension + Pulsatile Abdominal mass

7) Reactive Arthritis
Can’t See (Conjunctivitis) + Can’t Pee (Urethritis) + Can’t Climb a Tree (Arthritis)

8) Triad of Opioid Overdose
Pinpoint pupils + Respiratory Depression + CNS Depression

9) Hakims Triad – Normal Pressure Hydrocephalus
Gait Disturbance + Dementia + Urinary Incontinence

10) Horner’s Syndrome Triad
Ptosis + Miosis + Anydrosis

11) Mackler’s Triad – Oesophageal Perforation (Boerhaave Syndrome)
Vomiting + Lower Thoracic Pain + Subcutaneous Emphysema

12) Pheochromocytoma
Palpitations + Headache + Perspiration (Diaphoresis)

13) Leriche Syndrome
Buttock claudication + Impotence + Symmetrical Atrophy of bilateral lower extremities

14) Rigler’s Triad – Gallstone ileus
Gallstones + Pneumobilia + Small bowel obstruction

15) Whipple’s Triad – Insulinoma
Hypoglycemic attack + Low glucose + Resolving of the attack on glucose administration

16) Meniere’s Disease
Tinnitus + Vertigo + Hearing loss

17) Wernicke’s Encephalopathy- Thiamine Deficiency
Confusion + Ophthalmoplegia + Ataxia

18) Unhappy Triad – Knee Injury
Injury to Anterior Cruciate Ligament + Medial collateral ligament + Medial or Lateral Meniscus

19) Henoch Schonlein Purpura
Purpura + Abdominal pain + Joint pain

20) Meigs Syndrome
Benign ovarian tumor + pleural effusion + ascites

21) Felty’s Syndrome
Rheumatoid Arthritis + Splenomegaly + Neutropenia

22) Cauda Equina Syndrome
Low back pain + Bowel/Bladder Dysfunction + Saddle Anesthesia

23) Meningitis
Fever + Headache + Neck Stiffness

24) Wolf Parkinson White Syndrome
Delta Waves + Short PR Interval + Wide QRS Complex

25) Neurogenic Shock
Bradycardia + Hypotension + Hypothermia

Further Reading

Cite this article as: Sumaiya Hafiz, UAE, "Triads in Medicine – Rapid Review for Medical Students," in International Emergency Medicine Education Project, June 12, 2020, https://iem-student.org/2020/06/12/triads-in-medicine/, date accessed: July 6, 2022

A Song of Ice and Fire

A Song of Ice and Fire

As the year comes to an end, the holidays approach and, for lots of people, it means traveling to different places around the world. For those who live in the southern hemisphere, like me, the summer comes with al power, with temperatures as high as 35°C (95°F) or 40°C (104°F). For those who live in the northern hemisphere, “the winter is coming” and bring with him temperatures below 0°C (32°F) in some places. With these temperature extremes, we have some conditions to have in mind when working in the ED. How to treat a homeless patient who has slept on the streets on a freezing night? And how about an elderly person who lay on the beach sand under a blazing sun?

Hyperthermia

What is hyperthermia?

By definition, hyperthermia is a condition when there is a failure of the body’s thermoregulatory mechanisms to handle extrinsic and intrinsic heat. It’s common to see the expression “Heat-related Illness” to describe the conditions associated to the exposure to environmental heat.

Physiology

The heat-related illness (HRI) develops following a progressive pattern, divided in 3 phases [1].

  • ACUTE PHASE: 
    • Activation of inflammatory mediators, especially in the blood vessels; 
    • Gastrointestinal tract hypoperfusion, leading to bacterial translocation
    • Respiratory alkalosis due to hyperventilation
  • ENZYMATIC PHASE:
    • Coagulopathy, leading to a hypercoagulability state 
    • Endothelial injury and microvascular thrombosis 
    • All of this leading to disseminated intravascular coagulation (DIC)
  • LATE PHASE:
    • Liver dysfunction secondary to DIC
    • Kidney failure due to dehydration and hypotension
    • CNS lesions leading to cerebral edema and hemorrhage 
    • Cardiovascular dysfunction, worsening hypotension and causing vasoconstriction

Risk Factors

  • Extremes of age
  • Obesity
  • Elevated humidity rate
  • Lack of acclimatization and/or fitness
  • Ambient temperature
  • Dehydration
  • Cardiovascular disease
  • Drugs/medication (i.e alcohol, diuretics, amphetamines)

Categories of heat illness

  • Minor Heat Illness:  
    • Heat cramps: Intermittent muscle cramps likely related to salt deficiency and muscular fatigue, although the exact mechanism is not well known.
    • Heat Edema: Swelling of the feet and ankles typically in non-acclimatized people
    • Heat Syncope: Similar to orthostatic hypotension, caused by the physiologic response to the heat: volume depletion, peripheral vasodilatation and a reduced vasomotor tonus. More common in elderly people.
    • Prickly Heat: cutaneous rash caused by pores and sweat gland obstruction
  • Heat Exhaustion:
    • Occurs with a moderate elevation in the body core temperature (<40°C or 104°F) – RECTAL temperature is the most reliable method (even though is a level C evidence)
    • Usually accompanied by symptoms related to conditions described in the Minor Heat Illness and other nonspecific symptoms like nausea/vomiting, weakness and headache
    • DOES NOT PRESENT WITH ALTERED MENTAL STATUS
  • Heat Stroke:
    • Body temperature above 40° (104°F) WITH ALTERED MENTAL STATUS
    • Target organ damage
    • Usually dry and pale skin, however athletes can present with warm and wet skin

Management

  • Primary, we need to proceed with the basic measures: secure airway, monitorize and place IV fluids in order to maintain a mean arterial blood pressure > 60 mmHg [2].
  • The second step is to perform a rapid cooling, targeting a temperature <39°C (102°F) in the first 30 minutes. After reaching this goal, the active cooling should be stopped in order to avoid overshoot hypothermia
    • Cold water immersion is the best method available (level C evidence) [3].
      • Treat shivering with benzodiazepines if needed (avoiding extra heat generation)
    • DO NOT USE ANTIPYRETICS, they are not effective in this scenario [4].

Disposition

  • Patients with heat stroke should be admitted to a ICU to monitoring organ dysfunction, electrolytes disturbances and rebound hypothermia.
  • Young and otherwise healthy patients with heat exhaustion can be discharged home 
  • Be aware for the risk of recurrent hyperthermia when considering discharge a patient (returning to the same ambient)

Hypothermia

What is hypothermia?

  • Condition in which the body loses heat at a higher rate than its capacity in maintain the core temperature or elevate the heat production
  • Clinically defined as unintentional decrease of body temperature below 35°C (95°F)
  • In other settings, we can talk about “secondary hypothermia”, when the patient has an impaired thermoregulation due to a clinical condition such as hypothyroidism, ketoacidosis, malnutrition etc – In this article we will focus on accidental hypothermia, related to environmental exposure

Physiology

  • Initially, the metabolic rate increases, peripheral blood flow is shunted towards vital structures, and shivering initiates to increase heat production
  • If these compensations are not enough, the body temperature continues to drop, with the CNS being affected when it reaches 35°C (95°F). 
  • Cardiovascular: initial increase in heart rate and blood pressure; however, as core temperature declines, progressive bradycardia and hypotension occurs. In more severe hypothermia, myocardial irritability increases, leading to a high risk of arrhythmias.
  • Oxygen consumption: At a temperature of 28°C (82°F), the oxygen consumption is decreased by 50%, leading to a protective effect in CNS and other vital organs – but just if it develops before asphyxia (there are several studies trying to better understand the role of hypothermia as a protective measure in cardiac arrest) [5].

Risk Factors

  • Fatigue
  • Sleep deprivation
  • Rain, wind and water immersion
  • Burn
  • Extremes of age
  • Trauma
  • Alcohol
  • Hypoglycemia
  • Hypothyroidism
  • Hyperthermia treatment (rapid cooling)

Classification

Stage 1: Mild Hypothermia

  • Core temperature: 32 – 35°C (90 – 95°F)
  • Initially presenting with tachycardia, hypertension, shivering and vasoconstriction
  • Gradually develops ataxia, poor judgement, amnesia, apathy, dysarthria

Stage 2: Moderate Hypothermia

  • Core temperature 28 – 32°C (82 – 90°F)
  • Loss of shivering, lethargy, mydriasis, hyporeflexia, alterations in cardiac rhythm (Osborne J waves on EKG)

Stage 3: Severe Hypothermia

  • Core temperature: 24 – 28°C (75 – 82°F)
  • Hypoventilation, ventricular fibrillation, acid-basic disturbances, anesthesia, pulmonary edema 

Stage 4: Profound Hypothermia

  • Core temperature: below 24°C (75°F)
  • Oliguria, fixed pupils, asystole, apnea, coma 
  • Curiosity: 13,7°C (56,7°F) is the lowest temperature registered at which CPR was performed with satisfactory results [6].

Management

  • The first thing we need to do is to stop the cooling process 
    • Remove the environmental factor (take the patient out of the street, take off wet clothes etc.)
    • Try stop heat loss, putting up barriers like warm clothes, blankets, sleep bags, etc
  • Second step, we should identify the degree of hypothermia to guide our approach:
    • For Mild hypothermia, besides the strategies described before, we need to offer calories (food and warm drinks), monitoring for at least 30 minutes and warm the trunk
    •  [F]or Moderate hypothermia, we also need to keep the patient laid down and still, start volume reposition with warm fluids (40 – 42°C/104 – 107°F), Avoid food and beverage.
    • For Severe hypothermia: All the above and check for pulse and breathing – of pulse/breathing is absent, START CPR. – Consider transferring to a facility where ECMO is available
      • ECMO is the best option for severely hypothermic patients without signs of life who do not respond to initial resuscitative efforts. It has been shown to improve neurologically intact survival (48% to 63% survival with ECMO, <37% without ECMO) [7]. 

 “Nobody is dead until warm and dead”

Patients with core temperatures of <28°C have decreased electroencephalographic activity and loss of brainstem and pupillary reflexes, all of which may mimic death. Because of that, the patient can not be considered “dead” until his body temperature reaches at least 32°C.

Some conditions allow us to presume death even in patients with body temperature below 32°C and no vital signs: obvious lethal injury (i.e. decapitation), frozen body, potassium > 12, avalanche victims with burial > 35min or airway packed with snow.

References and Further Reading

The primary reference for this article was the recently launched book: “Medicina em Áreas Remotas no Brasil” (Wilderness Medicine in Brazil): JULIANA R. M. SCHLAAD e SASCHA W. SCHLAAD, Medicina em Áreas Remotas no Brasil, 1ed, Barueri (SP), Manole, 2020

Other sources of information as numbered and referred in the text:

  1. Powers SK, Howley ET. Regulação de temperatura. In: Powers SK, Howley ET. Fisiologia do exercício: teoria e aplicação ao conhecimento e ao desempenho. 9ed. Barueri: Manole; 2017. p.261-281.
  2. Tran TP. Heat emergencies. In: Ma OJ, Cline DM, ed. Emergency medicine manual. 6th ed. McGraw-Hill, NY: 2004:564-565
  3. Becker J, Stewart L. Heat-related illness. Am Fam Physician. 2011;83(11):1325-1330
  4. Lipman GS, Eifling KP, Ellis MA, Gaudio FG, Otten EM, Grissom CK. Wilderness medical society practice guidelines for the prevention and treatment of heat-related illness: 2014 update. Wilderness Environ Med. 2014; 25:S55-S65
  5. Soar J, Perkins G, Abbas G, et al. European Resuscitation Council Guidelines for Resuscitation 2010 Section 8. Cardiac arrest in special circumstances: Electrolyte abnormalities, poisoning, drowning, accidental hypothermia, hyperthermia, asthma, anaphylaxis, cardiac surgery, trauma, pregnancy, electrocution. Resuscitation. 2010;81(10):1400-1433.
  6. M. Gilbert, R. Busund, A. Skagseth, Nilsen PÅ, J.P. Solbø Resuscitation from accidental hypothermia of 13.7 degrees C with circulatory arrest Lancet, 355 (2000), pp. 375-376
  7. Brown DJ et al. Accidental hypothermia. NEJM 2012; 367(20): 1930-1938. PMID: 23150960
Cite this article as: Arthur Martins, Brasil, "A Song of Ice and Fire," in International Emergency Medicine Education Project, December 25, 2019, https://iem-student.org/2019/12/25/a-song-of-ice-and-fire/, date accessed: July 6, 2022

A Farmer’s Dilemma

Farmer's Dilemma

Case Presentation

It was a rainy night preceding my morning shift as a year 3 EM resident at one of our training centers in Abu Dhabi. The paramedics barged in with an agitated patient, who was found soaking wet in a farm field.

According to brief history that we got from the paramedics, the patient works at a farm and his boss found him collapsed, cold to touch and confused in the early morning hours. Paramedics also reported a confused, hypothermic, and tachycardic patient. They brought him directly to the ED, with no accompanying friends or family.

As we proceeded to resuscitate the patient, we noted that his initial vital signs did confirm hypothermia of 32 Celsius measured rectally, tachycardia, hypertension, and normal O2 saturation. We hooked him to the monitor, removed his wet clothing, gained IV access, started him on warm IV fluids, and covered him with blankets and a warming Bair Hugger (a warming blanket system).

Physical Exam

The patient was confused, agitated and uttering incomprehensive words, with a GCS of 11 (E3 V3 M5). I proceeded to examine him looking for more clues of why he was laying semiconscious under the rain all night. Systematic physical examination revealed pinpoint pupils, frothing and excessive salivations. Furthermore, diffuse mild crackles were noted on chest auscultation, and he was tachycardic with a regular rate and rhythm. Remaining physical exam was unremarkable, and a complete neurological exam was challenging.

Differential Diagnosis and Workup

Thinking of a broad differential diagnosis of altered mental status, systematic consideration of all possible etiologies similar to our patient presentation was reviewed. We have considered metabolic derangements, head trauma, CNS causes such as seizures and post-ictal status, infectious causes such as pneumonia or meningitis, and toxicologic causes, such as alcohol withdrawal, or medications overdose.

You may find useful this mnemonic for altered mental status!

ALTERED MENTAL STATUS

Further management plan included giving him benzodiazepines for the agitation and possible post-ictal status. We collected basic blood work and proceeded for a head CT to rule out traumatic or atraumatic intracranial pathologies. Blood workup was inclusive of an alcohol level, Aspirin, Acetaminophen level, and a urine toxicology screen.

As the patient returned from the CT, he apparently had passed the copious amount of loose stools, that smelled surprisingly like garlic that studded the ED with its smell.

The head CT was normal, and most of his blood workup came back unremarkable. But, he remained confused and agitated as the benzodiazepines were wearing off and despite all the warming measures. ECG showed only sinus tachycardia, and a chest X-Ray was unremarkable.

smells like garlic!

What do you think? What are the causes for this?

agents smells like garlic

phosphorus, tellurium, inorganic arsenicals and arsine gas, organophosphates, selenium, thallium, dimethyl sulfoxide
Learn More

The garlic smell did give us a lead though, we thought further of possible toxic agents that may give such a smell, along with a consistent similar clinical picture.

Case Management and Disposition

Collecting our clues once more, we had pinpoint pupils, frothing, salivation, wet lungs, vomiting and loose motions. Patient’s collective symptoms and signs indicated a Cholinergic Toxidrome, possibly due to Organophosphates ingestion.

The patient was already decontaminated with removal of all his clothes. All healthcare providers were equipped with personal protective equipment.

This was confirmed an hour later when his farm owner showed up with a Pesticides Bottle that he found near him in the early morning hours before calling an ambulance. Pesticide is shown in Figure. The content of the bottle is consistent with Organophosphates Toxicity, and hence his Cholinergic Toxidrome.

Pesticide Bottle Found Next To The Patient.
Pesticide Bottle Found Next To The Patient.

He was started on Atropine, and Pralidoxime, assessed and admitted to the ICU with arranged psychiatric consult to assess his suicidal ideations once he stabilizes.

Critical Thinking and Take-home Tips

A collection of symptoms and physical signs caused by a certain toxic agent.

Cholinergic
Anticholinergic
Sedative/Hypnotic
Sympatholytic
Sympathomimetics

Cholinergic toxicity represents a cholinesterase inhibitor poisoning. It results from the accumulation of excessive levels of acetylcholine in synapses. Clinical picture resulting from the Acetylcholine build up depends on the type of receptors that it stimulates and where is it found in the body. It can stimulate the nicotinic and muscarinic receptors. The balance of these stimulations reflects such clinical presentations.

Think of the symptoms that can be caused depending on the type of receptors affected by the buildup of acetylcholine.

Muscarinic Receptors – SLUDGE(M)

  • Salivation
  • Lacrimation
  • Urination
  • Diarrhea
  • Gastrointestinal pain
  • Emesis
  • Miosis

Nicotinic Receptors (NMJ) – MTWThF

  • Mydriasis/Muscle cramps
  • Tachycardia
  • Weakness
  • Twitching
  • Hypertension
  • Hyperglycemia
  • Fasciculations

These are called the Killers B’s which consist of Bradycardia, Bronchorrhea and Bronchospasm.

Decontamination should always be considered first in all cases with possible hazardous exposure from the patient and his environment to all health care providers in contact with him. All caregivers should wear appropriate personal protective equipment’s and make sure to remove all clothing and possible objects with the suspected contaminant.

Supportive care is a cornerstone to all unstable patients, make sure that they are monitored, with proper IV access and supplemental oxygen as needed.

Furthermore, airway management is lifesaving in similar patients, as bronchorrhea is one of the killer B’s and can lead to high fatality.

Antidotes such as Atropine and Pralidoxime in Cholinergic toxicity are paramount, as they help reverse the etiology, and prevent further worsening of the toxicity.

Make sure that such patients are admitted under needed specialty care with proper observation and reassessment for the patient.

Consult a toxicologist if feasible in your center to provide you with further management details and interventions that can help your patients better.

Conclusion

Organophosphates can be found in pesticides, chemical weapons such as nerve gases, and few medications as well such as neostigmine or edrophonium. They are highly lipid soluble making them easily absorbed via breathing and skin contact as well. Encountering similar patients, it is quite important to always be systematic in your approach, resuscitate your patient first, and make sure to use your history taking as feasible and physical examination to collect all the clues needed to narrow down your differentials and find the most appropriate treatment needed for your patient.

References and Further Reading

  1. Organophosphate toxicity on WikEM: https://www.wikem.org/wiki/Organophosphate_toxicity
  2. Das RN, Parajuli S. Cypermethrin poisoning and anti-cholinergic medication- a case report. Internet J Med Update. 2006;1:42–4.
  3. Aggarwal, Praveen et al. “Suicidal poisoning with cypermethrin: A clinical dilemma in the emergency department.” Journal of emergencies, trauma, and shock vol. 8,2 (2015): 123-5. doi:10.4103/0974-2700.145424
  4. Lekei EE, Ngowi AV, London L. Farmers’ knowledge, practices and injuries associated with pesticide exposure in rural farming villages in Tanzania. BMC Public Health. 2014;14:389. Published 2014 Apr 23. doi:10.1186/1471-2458-14-389

Suggested Chapters and Posts in iEM

Cite this article as: Shaza Karrar, UAE, "A Farmer’s Dilemma," in International Emergency Medicine Education Project, July 19, 2019, https://iem-student.org/2019/07/19/a-farmers-dilemma/, date accessed: July 6, 2022

A new chapter is added – Drowning

drowning!

Drowning chapter written by Ana Spehonja from Slovenia is just uploaded to the Website!