Case summary: Today, our stellar sub-I, Caroline Opene, presented a case in its early stages that was ripe with higher-order learning. A 68M with a PMH homelessness and EtOH abuse, with recent 1/2 blood cultures positive for staph epi, who presented with abrupt-onset nausea/vomiting, and was found to have fever and leukocytosis.
- A history of the abrupt onset of a symptom should trigger you to think about 5 broad categories: vascular events, electrical events, molecule release, perforation, obstruction
- Nausea/vomiting are non-specific signs of pathology along the vagal nerve pathway. Searching for a 3rd associated symptom (e.g. eye pain, chest pain) can help localize along the tract and guide your inquiry (e.g. glaucoma, ACS).
- Recall the non-infectious causes of fever: clot (usually low-grade), meds/tox (including withdrawal), autoimmune (including gout), malignancy, organ inflammation
- Important to note that our definition of abrupt-onset may be different from what patients experience, so this history can be difficult to obtain
- However, when an abrupt time course is elicited, consider using this framework:
- vascular event (e.g. thunderclap headache in subarachnoid hemorrhage)
- electrical event (e.g. abrupt onset of tachycardia in ARNRT)
- molecule release (e.g. histamine release in anaphylaxis)
- perforation (e.g. abdominal pain in ruptured peptic ulcer)
- obstruction (e.g. abdominal pain and vomiting in incarcerated hernia)
Neurocircuitry of nausea/vomiting:
- Although the pathophysiology of nausea/vomiting is quite complex, it is helpful to think of the vagal nerve as being the pathway along which pro-emetic input and output travels.
- Apologies in advance to the neurologists reading this blog, but here is a quick overview:
- the vagal nerve transmits chemical and motor pro-emetic signals from the abdominal viscera to the nucleus tractus solitarius (NTS)
- the NTS integrates these signals with information from other CNS sites (vestibular, cerebellar, cortex, limbic system, area prostema)
- the NTS sends these integrated pro-emetic signals via the vagus nerve
- the vagus nerve mediates the autonomic nervous system output that leads to the symptoms of nausea (sweating, pallor, salivation, increase in blood pressure, tachycardia, cutaneous vasoconstriction, decreased gastrointestinal motility)
- this signaling involves lots of neurotransmitters that are the target of many of our anti-emetic medications
- Thus, when a patient presents with nausea/vomiting, we are often taught to consider a vast array of etiologies, and the “third symptom” can guide us to where along the path of the vagal nerve input/output tract to investigate more fully
- Gut/peritoneum: obstruction, functional disorders, IBS, PUD, cholecystitis, pancreatitis, gastroparesis
- CNS: migraine, increased ICP, glaucoma
- Labyrinthine disorders: motion sickness
- Endocrine/metabolic: Pregnancy, uremia, DKA, adrenal insufficiency
- Meds/tox: opiates, chemotherapy, EtOH
- Cardiovascular: ACS, cardiogenic shock
Babic T, Browning KN. The role of vagal neurocircuits in the regulation of nausea and vomiting. European journal of pharmacology. 2014;722:38-47. doi:10.1016/j.ejphar.2013.08.047.
Singh P, Yoon SS, Kuo B. Nausea: a review of pathophysiology and therapeutics. Therapeutic Advances in Gastroenterology. 2016;9(1):98-112. doi:10.1177/1756283X15618131.
Quigley, Eamonn M.M. et al. AGA technical review on nausea and vomiting. Gastroenterology , Volume 120 , Issue 1 , 263 – 286
Non-infectious causes of fever:
After ruling out infection, you can burn this list in your brain
- Clot (typically low-grade)
- Malignancy (typically low-grade)
- Central fever
- Organ inflammation (pancreatitis, alcoholic hepatitis)
- Autoimmune disease (we discussed polyarticular gout)
- Meds/toxins (drug fever, NMS, serotonin syndrome, stimulants, EtOH withdrawal)