Healthy Patients with Potential to Crash

Authors: Daniel Ritter (Medical Student, The Ohio State University College of Medicine) and Mark J Conroy, MD (Assistant Professor of EM, The Ohio State University Wexner Medical Center, @mjconroy_md) // Edited by: Jennifer Robertson, MD, MSEd and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

 Introduction

A 30-year-old healthy female presents to the emergency department (ED) complaining of nausea, vomiting, and diarrhea that have worsened over the last 24 hours. She admits to some lightheadedness and states that she feels “just out of it”.  She denies any abdominal pain or blood in her emesis and stool. Some coworkers have been out sick with similar symptoms following a company party over the weekend.  She takes “some pill” for a “gland problem”, but she lost the bottle a few days prior.

The patient’s initial vital signs include a heart rate of 105 beats per minute (bpm) and a blood pressure of 90/50 mmHg. The patient is physically fit and reports that her blood pressure always runs on the “low side”. Her examination reveals dry mucous membranes and tachycardia but it is otherwise normal.  The patient has no neck stiffness, cardiac murmurs, abdominal pain, or rashes. You order routine laboratory tests and and treat her symptoms with an antiemetic and intravenous (IV) fluids.

After about 30 minutes, the patient’s chemistry returns and demonstrates a marked hyperkalemia and hyponatremia. When you reassess the patient, you note that she has an altered mental status and her blood pressure is 72/40 mmHg.

Unhealthy healthy patients

One of the first steps in any ED evaluation is differentiating between those patients who are sick and those who are not sick. While a lifetime of patient care can make this a subconscious decision for most emergency providers, the process is still subjective. Criteria, algorithms, and/or clinical decision tools exist for many scenarios, but not all. It is especially difficult for clinicians to determine the severity of an illness in an otherwise young healthy patient with non-specific symptoms.

Among every group of nonspecific presentations is a new (or overlooked) diagnosis that, if missed, can seriously harm or even kill a patient. The goal of training and lifetime learning is for emergency physicians to become experts at teasing out those who are covertly sick. Several of the conditions discussed below can easily be overlooked because they may present, at least initially, with non-concerning symptoms. However, they have the ability to cause serious harm.

Acute Adrenal Insufficiency (Adrenal Crisis)

Background

Adrenal insufficiency is divided into three categories: primary, secondary, and tertiary.1  Primary disease is due to intrinsic problem(s) with the adrenal cortex, while secondary adrenal insufficiency is due to pituitary failure or a lack of responsiveness of the adrenal glands to adrenocorticotropic hormone (ACTH). Tertiary adrenal insufficiency is due to the impaired hypothalamic production or action of ACTH, vasopressin or both.1

Adrenal crisis can occur as an exacerbation of any chronic cause of adrenal insufficiency, or as an abrupt injury to any component of a healthy adrenal axis.  Common causes include abrupt cessation of exogenous glucocorticoid use, bilateral adrenal infarction/hemorrhage, or acute stress in the setting of previously undiagnosed chronic adrenal insufficiency.2

How it presents

Acute adrenal insufficiency can present with hypotension, abdominal pain and/or rigidity, nausea, vomiting, and fever due to coexisting infection.  Hyperpigmentation may be a feature of those with chronic adrenal insufficiency.  A history of chronic fatigue or abrupt cessation of chronic glucocorticoid use could be present depending on the etiology.2

Why the diagnosis can be challenging

Acute adrenal insufficiency is rare. The risk of developing acute adrenal insufficiency in a patient with chronic adrenal insufficiency is about 6-10 per 100 patient-years.3  It can also be easily overlooked as a diagnosis early on in a patient’s presentation.  Furthermore, endocrine causes of hemodynamic instability are not generally considered to be one of the four main categories of shock (obstructive, cardiogenic, distributive, and hypovolemic).  These factors can delay diagnosis and lead to worsening crisis before appropriate treatment is initiated.

How to catch it

A more thorough history can be key in identifying the right track for the emergency physician. Routine laboratory analysis often reveals hyperkalemia and hyponatremia.2 Patients in adrenal crisis face significant morbidity and mortality. Immediate treatment with fluid resuscitation and steroid replacement (dexamethasone 4-10 mg IV when no prior diagnosis exists4, otherwise hydrocortisone 100 mg IV or IM, with 100-300 mg every day thereafter for the duration of treatment2) is necessary before receiving confirmatory diagnostic tests in patients who are at risk.2

Other pearls

Cessation of inhaled glucocorticoids can precipitate acute adrenal insufficiency.5

Acute Pancreatitis

Background

A condition involving inflammation, and often hemorrhagic necrosis, of the pancreatic parenchyma. Several causes exist but gallstone obstruction of the pancreatic duct, metabolic/hereditary disorders, and alcohol use most commonly underlie this painful condition6.  In necrotizing pancreatitis, mortality can be as high as 17%.7 Severe cases can lead to marked hypotension and end-organ failure.6

How it presents

About 50% of the time, patients present with severe, persistent epigastric pain radiating to the back.8 Pain is usually associated with severe nausea and vomiting.6

Why the diagnosis can be challenging

The differential diagnosis for patients with abdominal pain is, unfortunately, very broad.  Epigastric pain could be the manifestation of intra-abdominal, cardiac, or intra-thoracic processes. In addition, pancreatitis due to alcohol or metabolic disorders can have a more gradual onset with poor localization of pain.  Degree of pain is also variable, and some patients may not be as uncomfortable as others.  In a patient who is otherwise healthy, and who presents with gradual onset, localized and unimpressive epigastric pain, acute pancreatitis could easily be missed.

How to catch it

Keeping broad differential diagnoses for patients with abdominal pain is key.  Consider abdominal computed tomography (CT) for lipase (+/ amylase) levels that are only mildly elevated, or with atypical presentations not otherwise explainable.

Other pearls

Acute pancreatitis on ultrasound appears enlarged and heterogeneous.  Hypoechoic fluid may be visualized, as well as gallstones in the gallbladder or common bile duct.9

Arrhythmia

Background

Abnormal cardiac rhythms vary in pathophysiology, appearance on electrocardiogram (ECG), and lethality.  They can range from benign ectopic beats (like PVCs) to very dangerous (like atrial fibrillation in patients with Wolff-Parkinson-White).

How it presents

Presenting symptoms are variable and can include palpitations, anxiety, syncope, dizziness, chest pain, and shortness of breath.

Why the diagnosis can be challenging

The difficulty is not in obtaining the ECG but instead the interpretation. Outside of the overt arrhythmia, ECG signs of channelopathy or structural abnormality in asymptomatic patients can easily be overlooked.

 How to catch it

Key features on ECG for high-risk syndromes include:

  • Long QT interval: A sign of the aptly named Long QT Syndrome. It can be congenital or can be acquired in the setting of electrolyte abnormalities or certain pharmacologic agents.  A long QT interval puts patients at risk for sudden cardiac death due to Torsades de pointes.10
  • Delta wave: Classic for Wolff-Parkinson-White syndrome. The “slurring” of the R wave is a sign of an accessory pathway, which can lead to an unstable tachycardia (rate often greater than 200), cardiovascular instability and death.11
  • Q waves, atrial enlargement, left axis deviation, inverted T waves: In a young, healthy patient, any of these could be a sign of hypertrophic cardiomyopathy. Look for signs of structural changes, such as P wave abnormalities suggesting atrial enlargement.  Hypertrophic cardiomyopathy is the most common cause of sudden cardiac death in young athletes.12
  • Pseudo-right bundle branch block and ST elevation in V1 and V2: Suggestive of Brugada syndrome, a sodium channelopathy. ST elevation can be divided into two patterns: type 1 features a convex, descending ST segment followed by an inverted T-wave, and type 2 features a “saddle-back” ST-T morphology.  A third type exists involving the criteria of Type 1 & 2 but with < 2 mm of elevation. Brugada syndrome predisposes patients to sudden-onset ventricular tachyarrhythmias.13

Other pearls

Often genetic, but not always, a family history is very helpful for assessing risk for different arrhythmias.

Substance Abuse

Background

Overdoses and withdrawal are an increasingly large burden on emergency medical service (EMS) providers and emergency departments as newly synthesized illicit drugs are abused and opioid addiction across the United States grows.14

How it presents

Signs and symptoms of overdose or withdrawal depends on the substance in question.  Some common examples include:

  • Opioids
    • Intoxication: Respiratory depression, altered mental status, bradycardia, miotic pupils.15,16
    • Withdrawal: Dysphoria, restlessness, myalgias/arthralgias, nausea, vomiting, tachycardia, diarrhea.16
  • Cocaine
    • Intoxication: Hypertension, tachycardia, mydriatic pupils, agitation.16,17
    • Withdrawal: Depression/anxiety, fatigue, anhedonia, increased sleep.18
  • Amphetamines
    • Intoxication: agitation/psychosis, tachycardia, hypertension, mydriatic pupils, diaphoresis.19
    • Withdrawal: dysphoria, fatigue, increased sleep, anxiety.18,19
  • Phencyclidine (PCP)
    • Intoxication: Hypertension, hallucinations, nystagmus, tachycardia, agitation.20
    • Withdrawal: Confusion, anxiety, depression, memory loss.19
  • Alcohol
    • Intoxication: Slurred speech, nystagmus, unsteady gait, nystagmus, disinhibition.21
    • Withdrawal: Insomnia, tremulousness, hallucinations, headache, diaphoresis, seizures, delirium tremens.22,23

 Why the diagnosis can be challenging

Intoxication or overdose from alcohol or drugs can be easy to diagnose with sufficient history.  Otherwise, an acutely altered patient with little available history can be a diagnostic challenge. Additional conditions can also be overlooked in the patients – head trauma following opiate and alcohol abuse, myocardial infarction with cocaine intoxication, or delirium tremens in a patient with no known history of alcohol abuse.

 How to catch it

Whenever possible, accurately identify the substance in question in order to prepare for potentially dangerous sequelae.  Try to keep a wide differential in patients who are altered or agitated.

 Other pearls

Remember to ask about alcohol, tobacco, and drug use in all patients.

Crush Injury

Background

The development of rhabdomyolysis and acute kidney injury in the setting of a crush injury is well-known. A more severe results of crush injury can occur in disaster victims who become trapped in fallen structures. In this case, these victims can often become hypotensive following extrication due to third-spacing of fluids into the freed crushed tissue. Thus, compartment pressures should be monitored closely in these patients.24,25

 How it presents

Providers in the field will most often encounter hypotensive patients following a crush injury.  However, providers in the ED should be aware of this possibility when caring for victims of natural or man-made disasters.

 Why the diagnosis can be challenging

Providers in the field must be aware of the dangers of crush injuries beyond the direct trauma to limbs.  If an IV is not placed and fluids not started before extrication, deterioration should be an ongoing concern. Additionally, it is possible that a provider in the emergency department setting could be unaware of a crush injury in a hypotensive trauma patient, prompting him or her to look for other causes of hypotension.

 How to catch it

When dealing with entrapped victims, an IV line and fluids should be started before extrication whenever possible.  This can prevent post-extrication hypotension as well as ameliorate the potential for acute kidney injury (AKI).25

 Other pearls

Bicarbonate and mannitol (1 amp and 10 g IV, respectively, during extrication) can be used to avoid AKI following crush injury.24

Heat Illness

Background

Heat illness is considered a failure of the body’s thermoregulatory system to handle intrinsic and extrinsic heat. It can be further classified based on signs and symptoms. Syncope, muscle cramps, heat exhaustion are all part of the spectrum of heat related illness, with heat stroke having the highest rates of morbidity and mortality.26

How it presents

Heat illness can affect populations of all ages, from very young to very old. Typically, younger patients present following a period of exertion.  Any rectal temperature greater than 104° Fahrenheit (F) with mental status changes necessitates active cooling. For patients with a temperature less than 104° but still greater than 98.6°, active cooling (ice water immersion, cooling mattress, etc) should seriously be considered. Passive cooling (removing the patient from the warm environment, getting rid of wet clothing, and hydration) is still a must. Rechecking a rectal temperature to ensure improvement is also necessary as some patients can continue increasing early on before passive methods have taken effect.

Why the diagnosis can be challenging

Older patients often present with heat illness without any preceding exertion. Often left unattended in the heat as well as additional medications complicating the diagnosis, these patients present with little to no history to direct your evaluation and treatment. Additionally, these patients can suffer from secondary electrolyte and cardiovascular complications. 26

How to catch it

Obtaining a rectal temperature is the gold standard when evaluating patients for heat illness. Keep heat illness in your list of differential diagnoses, especially when working on days with high heat indices or an endurance event nearby.

Other pearls

Ice packs in the axillae and groin as well as evaporative cooling with misting and a fan are the most feasible cooling options in the ED. Cold water immersion is the gold-standard when working events. Goal rate for cooling is 1° (F) every 3 minutes.  Antipyretics are not useful for decreasing temperature in these patients.27,28

“Vitals are vital” and “Keep your differential broad”

Providers have heard these phrases repeated since beginning medical school, and nowhere are they more applicable than when dealing with young healthy patients.

Abnormal vital signs need to be explained within the clinical context.  Hydration status can be an easy go-to for tachycardia but anchoring can lead you down the wrong diagnosis and treatment pathways if other alternative causes are not considered. In the case at the start of this post, symptomatic hypotension and an unclear medication history are key red flags that should not be overlooked.

Finally, when a patient does not respond as you expect (improved heart rate with IV fluids, decreased pain with medication, etc.) emergency providers should step back and re-evaluate. Make sure you have considered all life threatening diagnoses and that you have adequately evaluated patients for these diagnoses. Not every potential diagnosis needs to be tested for. However, considering the diagnosis is important because it helps avoid bias and potentially, missed diagnoses.

Pearls

Address abnormal vital signs or have a cohesive explanation as to why you are not addressing them.

Abnormal vital signs without a clear explanation, as well as vital signs that do not resolve with treatment, should prompt expanded consideration of the patient’s complaint, further investigation, and likely both.

-Bad things happen and even healthy people get sick.

References / Further Reading

1Charmandari E, Nicolaides NC, Chrousos GP. Adrenal insufficiency. The Lancet. 2014;383(9935):2152-2167.

2Puar TH, Stikkelbroeck NM, Smans LC, Zelissen PM, Hermus AR. Adrenal Crisis: Still a Deadly Event in the 21st Century. The American Journal of Medicine. 2016;129(3).

3Arlt W, Allolio B. Adrenal insufficiency. The Lancet. 2003;361(9372):1881-1893.

4Asare K. Diagnosis and Treatment of Adrenal Insufficiency in the Critically Ill Patient. Pharmacotherapy. 2007;27(11):1512-1528.

5Piédrola G, Casado JL, López E, Moreno A, Perez-Elías MJ, García-Robles R. Clinical features of adrenal insufficiency in patients with acquired immunodeficiency syndrome. Clinical Endocrinology. 1996;45(1):97-101.

6Lankisch PG, Apte M, Banks PA. Acute pancreatitis. The Lancet. 2015;386(9988):85-96.

7Banks PA, Freeman ML. Practice Guidelines in Acute Pancreatitis. The American Journal of Gastroenterology. 2006;101(10):2379-2400.

8Banks PA. Acute pancreatitis: Diagnosis. In: Pancreatitis, Lankisch PG, Banks PA (Eds), Springer-Verlag, New York 1998. p.75.

9Bollen TL, Santvoort HCV, Besselink MG, Es WHV, Gooszen HG, Leeuwen MSV. Update on Acute Pancreatitis: Ultrasound, Computed Tomography, and Magnetic Resonance Imaging Features. Seminars in Ultrasound, CT and MRI. 2007;28(5):371-383.

10Khan IA. Long QT syndrome: Diagnosis and management. American Heart Journal. 2002;143(1):7-14.

11Bhatia A, Sra J, Akhtar M. Preexcitation Syndromes. Current Problems in Cardiology. 2016;41(3):99-137.

12Elliott P, Mckenna WJ. Hypertrophic cardiomyopathy. The Lancet. 2004;363(9424):1881-1891.

13Littmann L, Monroe MH, Kerns WP 2nd, Svenson RH, Gallagher JJ. Brugada syndrome and “Brugada sign”: clinical spectrum with a guide for the clinician.  Am Heart J. 2003 May; 145(5):768-78.

14Rudd RA, Aleshire N, Zibbell JE, Gladden RM. Increases in Drug and Opioid Overdose Deaths — United States, 2000–2014. MMWR Morbidity and Mortality Weekly Report. 2016;64(50-51):1378-1382.

15Sporer KA. Acute Heroin Overdose. Annals of Internal Medicine. 1999;130(7):584.

16Hughes JR, Higgins ST, Bickel WK. Nicotine withdrawal versus other drug withdrawal syndromes: similarities and dissimilarities. Addiction. 1994;89(11):1461-1470.

17Merigian KS, Roberts JR. Cocaine Intoxication: Hyperpyrexia, Rhabdomyolysis and Acute Renal Failure. Journal of Toxicology: Clinical Toxicology. 1987;25(1-2):135-148.

18Lago JA, Kosten TR. Stimulant withdrawal. Addiction. 1994;89(11):1477-1481.

19Khantzian EJ. Acute Toxic and Withdrawal Reactions Associated with Drug Use and Abuse. Annals of Internal Medicine. 1979;90(3):361.

20Mccarron MM, Schulze BW, Thompson GA, Conder MC, Goetz WA. Acute phencyclidine intoxication: Incidence of clinical findings in 1,000 cases. Annals of Emergency Medicine. 1981;10(5):237-242.

21Camí J, Farré M. Drug Addiction. New England Journal of Medicine. 2003;349(10):975-986.

22Etherington JM. Emergency management of acute alcohol problems Part 1: Uncomplicated withdrawal. Canadian Family Physician. 1996;42:2186-2190.

23Ferguson JA, Suelzer CJ, Eckert GJ, Zhou X-H, Diffus RS. Risk factors for delirium tremens development. Journal of General Internal Medicine. 1996;11(7):410-414.

24Gonzalez D. Crush syndrome. Crit Care Med. 2005 Jan;33(1 Suppl):S34-41.

25Sever MS, Vanholder R, Lameire N. Management of Crush-Related Injuries after Disasters. New England Journal of Medicine. 2006;354(10):1052-1063.

26Leon LR, Bouchama A. Heat Stroke. Comprehensive Physiology. March 2015:611-647.

27Bouchama A, Dehbi M, Chaves-Carballo E. Cooling and hemodynamic management in heatstroke: practical recommendations. Crit Care. 2007;11(3):R54

28Smith JE.  Cooling methods used in the treatment of exertional heat illness. Br J Sports Med. 2005;39:503-7.

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