top of page


The Best in FOAM Education

  • Alexander Bracey, MD

A Case of Profound Hypotension

I recently had the privilege of caring for a 40ish year old man, primarily Spanish speaking, who was obviously uncomfortable and appeared to be in distress. By way of an interpreter and through clenched teeth, he told me that he had been experiencing severe abdominal pain over the last 3 days. He had recently traveled to Texas and been diagnosed with a “liver infection” for which he had been on antibiotics. He had experienced loose, brown stool for the last 2 weeks. He had been started on an antibiotic, the name of which he could not recall, the week prior. He did not otherwise have any medical problems or take medications by his report.

On exam he was alert, in apparent distress and occasionally clutching his abdomen. He had generalized abdominal tenderness, though his abdomen was flat and without peritoneal signs or bruising. His skin was warm and dry, pulses intact in all extremities. He was tachycardic without abnormal heart sounds and his lung were clear.

His vital signs were as follows: 36.3 orally, RR: 28, HR: 123, SpO2: 100%, unable to detect BP with automated cuff. BP was 60/palp manually.

Take a minute to consider what your differential and management might be.


We ordered norepinephrine to be infused peripherally. He was felt to be overall fluid-down, and was empirically given 3L of Lactated Ringers, broad spectrum antibiotics, and laboratories including a lactate, VBG, and blood cultures were drawn and sent. RUSH exam revealed a normal heart without pericardial effusion and hyperdynamic LV function, no intraperitoneal fluid, and a normal sized aorta. His IVC was flat and lung sliding was present bilaterally. An upright chest XR was negative for pneumothorax, nor free peritoneal air. Meanwhile, a CT of the abdomen and pelvis with contrast was ordered.

Armed with a story of recent travel with profound diarrhea and a nebulous “liver infection,” I was prepared to declare this septic shock from a GI source and move along after he was stabilized. One thing continued to strike me as odd, however: how could this man continue to mentate and eloquently express his discomfort even in the setting of profound hypotension, which I had concluded from overwhelming sepsis?

The answer came from another member of the clinical team. A learner in the department who was looking back through the patient’s records while I conducted the H&P came to me and asked if this patient’s known history of Addison’s Disease might be contributing to his presentation today.

A bit on adrenal insufficiency / adrenal crisis:

  • Categorized as primary (adrenal disease), secondary (most commonly caused by cessation of exogenous steroids, also by pituitary disease), and tertiary (hypothalamic disease)

  • The most common inciting factor for adrenal crisis is fever or GI illness, though it can be brought about by any systemic insult (e.g., trauma, sepsis, surgery, GI bleeding, etc.)

  • The classic feature of adrenal crisis is profound hypotension that can be refractory to volume and vasopressor resuscitation which is due to vasoplegia brought on by mineralocorticoid deficiency. Abdominal pain is also common, along with a list of other general and nonspecific symptoms.

  • There is no specific diagnostic laboratory study to confirm the diagnosis in the immediate setting; however, if it is suspected then a mineralocorticoid (e.g., hydrocortisone, dexamethasone) is the first line therapy in addition to fluid resuscitation. Early initiation of pressors is indicated in the face of profound hypotension. Glucocorticoids (e.g., methylprednisolone, prednisone) will not treat the hypotension, as they have no mineralocorticoid effects!

  • Classic findings for adrenal insufficiency are seen on the chem panel: hyperkalemia, hyponatremia, hypoglycemia, though these findings may vary depending on the etiology of the deficiency.

Case resolution:

Feeling foolish, I asked the patient when the last time he last took his home steroids. He said that he had stopped taking them earlier in the week when he began taking the antibiotics. We administered hydrocortisone 100 mg IV and over the next 30 minutes the patient’s blood pressure became measurable and lingered around 100 systolic.

In this particular case, his potassium and glucose levels were normal; however, he was profoundly hyponatremic, the initial value at 108 mmol/L. Given that he was mentating normally and was neurologically intact, we simply fluid restricted the patient from receiving further crystalloids. The goal of should be to correct the hyponatremia by 6 mmol/L per day, unless there are severe features (e.g., seizure, focal neurological deficit, coma). In the latter example, increasing the sodium by 6 mmol/L in the first 6 hours and then stopping for the day will treat the severe features safely. The consequence of overshooting the correction is central pontine myelinolysis, a devastating disease.

This patient’s blood pressure continued to improve following hydrocortisone administration. His CT revealed a normal abdomen and pelvis. He had a brief ICU stay for monitoring of his blood pressure and electrolyte resolution. His sodium was gradually corrected over the subsequent 4 days and his blood pressure returned to normal ranges. He was seen by endocrine and was restarted on his home regimen of fludrocortisone, a PO mineralocorticoid. The importance of his life sustaining medication was reinforced and he was discharged to home 3 days after initial presentation.

Learning Points:

  1. In the critically ill patient always ask about recent use of systemic steroids.

  2. Review recent prior records when available.

  3. Resist early diagnostic closure and keep your differentials broad.

  4. When giving stress dose steroids, an agent with mineralocortiocoid activity (e.g., hydrocortisone, fludrocortisone) must be used, as it has effect on blood pressure via the RAAS system unlike glucocorticoids (e.g., prednisone, methylprednisolone).

  5. In hyponatremia, in general the treatment is: fluid restriction and gradual correction of the sodium.


Alexander Bracey is a third year resident and the QA/QI Chief at Stony Brook.



  1. Brit Long. emdocs - Adrenal Crisis in the ED.. emDocs. Published on May 15th 2015. Accessed on November 28th 2018, Available at []

  2. Tintinalli JE et al. Adrenal insufficiency and adrenal crisis. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 2011; 7.

  3. Scott Weingart. EMCrit Podcast 39 – Hyponatremia. EMCrit Blog. Published on January 17, 2011. Accessed on November 28th 2018. Available at [ ].

bottom of page