Case:

Ms. S is a 32-year-old woman who complains of nausea and vomiting. She reports that she felt well until 5 days ago when she noticed urinary frequency and burning on urination. She increased her intake of fluids and cranberry juice but noticed some increasing right back pain 2 days ago. Yesterday, she felt warm and noticed that she had a fever of 38.8°C and teeth-chattering chills. Subsequently, she has been unable to keep down any food or liquids and has persistent nausea and vomiting. She feels weak and dizzy.

Physical exam: supine BP, 95/62 mm Hg; pulse, 120 bpm; temperature, 38.9°C; RR, 24 breaths per minute. On standing, her BP falls to 72/40 mm Hg with a pulse of 145 bpm. Cardiac and pulmonary exam are notable only for the tachycardia. She has 2+ right costovertebral angle tenderness. Abdominal exam is soft without rebound, guarding, or focal tenderness. Initial laboratory results include Na+, 138 mEq/L; K+, 5.4 mEq/L; HCO3−, 14 mEq/L; Cl−, 102 mEq/L; BUN, 30 mg/dL; creatinine, 1.2 mg/dL; glucose, 90 mg/dL.

The patient denies any history of alcohol use, moonshine or antifreeze ingestion, or unusual salicylate use. Further lab studies include WBC, 18,500 cells/mcL with 62% granulocytes and 30% bands. Urinalysis reveals > 20 WBC/hpf.

Ms. S’s history does not suggest toxic ingestions and her history of fever, dysuria, and flank pain as well as leukocytosis and pyuria clearly suggest urinary tract infection and pyelonephritis. Her teeth-chattering chills suggest bacteremia, which combined with her hypotension suggests severe sepsis. Septic shock can cause lactic acid production and thereby generate an anion gap metabolic acidosis.

Ms. S was treated with broad-spectrum antibiotics and IV fluid resuscitation. After initial stabilization, hypotension recurred and urinary output dropped. She was transferred to the ICU. Four hours later her oxygenation deteriorated and a chest film revealed a diffuse infiltrate consistent with acute respiratory distress syndrome. She was intubated and given IV fluids, norepinephrine, antibiotics, mechanical ventilation, and activated protein C. Over the next 24 hours, her BP stabilized and her anion gap lactic acidosis resolved. Seventy-two hours later she was extubated. She eventually made a full recovery.

SOAP note:

S- 32 years old female, with no past significant medical history, presents herself with complains of nausea and vomiting. Ms.S states she noticed urinary frequency and burning sensation upon urination 5 days ago. 3 days ago, Ms.S also states she experienced increasing back pain after consumption of fluids such as cranberry juice. Ms.S also states that yesterday she had a fever of  38.8°C, and teeth-chattering chills. She denies any history of alcohol use, moonshine, salicylate use or antifreeze ingestion.

O- Supine BP, 95/62 mm Hg; pulse, 120 bpm; temperature, 38.9°C; RR, 24 breaths per minute. On standing, her BP falls to 72/40 mm Hg with a pulse of 145 bpm.

Cardiac and pulmonary exam are notable only for the tachycardia. 2+ right costovertebral angle tenderness.

Abdominal exam = soft without rebound, guarding, or focal tenderness.

Laboratory results = Na+, 138 mEq/L; K+, 5.4 mEq/L; HCO3−, 14 mEq/L; Cl−, 102 mEq/L; BUN, 30 mg/dL; creatinine, 1.2 mg/dL; glucose, 90 mg/Dl, WBC, 18,500 cells/mcL with 62% granulocytes and 30% bands. Urinalysis reveals > 20 WBC/hpf.

A- Ms.S history of fever, dysuria, pyuria and flank pain suggest urinary tract infection and pyelonephritis.

Also, her teeth-chattering chills with hypotension suggests sever sepsis.

P- 1) Broad-spectrum antibiotics +IV fluid resuscitation. (hypotension recurred + urinary output dropped)

2) Transfer to ICU

3) Incubate + IV fluid+ norepinephrine, antibiotics, mechanical ventilation, and activated protein C.

4) Full recovery after 72 hours.

Summary:

The leading hypothesis in this case were; cardiogenic shock, hypovolemic shock and septic. Patients who usually present with shock also have tachycardia and hypotension associated with them and often there’s a decrease of urinary output as well. In patients with septic shock, they usually appear with fevers, warm extremities, bounding pulses and tachypnea. Lastly those patients who present with cardiogenic/hemorrhagic shock also have cold extremities. Cardiogenic, hypovolemic shock and septic all fall under lactic acidosis which starts to develop when oxygen delivery in the cells is lacking. Insufficient amount of oxygen can lead to production of lactic acid via anaerobic metabolism. Lactate can build up in the body and cause the pH to decrease in the bloodstream. Another alternative differential for this patient was also Alcoholic ketoacidosis. Just like the name suggests, alcoholic ketoacidosis is caused to a combination of both alcohol effects and starvation on glucose metabolism. In alcoholic ketoacidosis, the levels of hepatic gluconeogenesis will decrease and the levels of insulin will therefore increase, and in turn will lead to increased lipolysis and impaired fatty acid oxidation. In our case, Ms.S denied any use of alcohol or any history of alcohol, therefore we can take off alcoholic ketoacidosis from our potential differential diagnosis

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