52 A 45-Year-Old Female With Nausea, Vomiting, and Abdominal Pain


Case 52

A 45-Year-Old Female With Nausea, Vomiting, and Abdominal Pain



Daniel Martinez



A 45-year-old female with a past medical history of type 1 diabetes mellitus (DM1) presents to the emergency room with 2 days of progressive nausea, vomiting, and abdominal pain. The patient is from Brazil and moved to the United States 3 years ago. Unfortunately, she lost her job and health insurance earlier this year, and she is recently homeless. During the past year, she was not able to eat well and ran out of insulin 1 week ago. She describes her abdominal pain as 5/10, pressurelike, generalized, nonradiating, and mildly worse with eating. In the emergency room, her blood pressure is 90/55 mm Hg, pulse rate is 125/min, respiration rate is 28/min, and temperature is 37.2 °C (99 °F). Her height is 5′4″ and weight is 120 pounds. She appears unwell, has dry mucus membranes, and has normal heart and lung sounds. Her abdomen is soft, mildly tender to palpation, but without rebound or guarding.



What is concerning about this presentation?


The patient’s history is very concerning for diabetic ketoacidosis (DKA). Her history of DM1 with decreased oral intake and a lack of insulin places her at high risk for DKA. Other causes of DKA include infection/sepsis, intoxication (alcohol/drugs), myocardial infarction, stroke, and pancreatitis.



Step 1


Basic Science Pearl


Patients with type 1 diabetes mellitus (DM1) are more at risk for developing DKA than patients with type 2 diabetes mellitus (DM2). This is because the pathophysiology of DKA involves severe insulin deficiency, which is rarer with DM2. This is because DM2 involves insulin resistance and relative insulin deficiency more so than an actual lack of insulin in the body. However, patients with DM2 can and do develop DKA during extreme conditions.



How should you begin workup of this patient?


There are three basic requirements to diagnose someone with DKA. There needs to be a plasma glucose >250 mg/dL, an anion gap acidosis with pH <7.3, and ketosis. The basic evaluation of DKA thus involves measuring a glucose finger-stick, a basic metabolic panel, arterial blood gas, and urinalysis.



You start a 2-liter normal saline bolus because she appears severely dehydrated on exam. Your nurse reports that the finger-stick blood glucose level is 550 mg/dL, which raises your suspicion for DKA. You then give 10 units of insulin intravenous (IV) push. Lab results become available: sodium 135 mEq/L, potassium 3.5 mEq/L, chloride 98 mEq/L, bicarbonate 15 mmol/L, blood urea nitrogen 25 mg/dL, creatinine 1.2 mg/dL, and glucose 600 mg/dL. The pH on the blood gas is 7.25, and ketones are found in the urinalysis. You then start an insulin drip, continue high-rate isotonic IV fluid resuscitation, and admit the patient to the medical intensive care unit.




Diagnosis: Diabetic ketoacidosis



What other abnormalities are found in DKA?


The pathophysiology of DKA involves far more than hyperglycemia and anion gap ketoacidosis. Another major pathology is the osmotic diuresis that occurs when blood glucose levels are consistently that high. As glucose is filtered into the renal tubules, it pulls in water and other important electrolytes with it. This causes severe polyuria/polydipsia, dehydration, hypokalemia, and hypomagnesemia. The treatment of DKA therefore commonly involves aggressive replacement of fluids and electrolytes.



Step 1/2/3


Basic Science/Clinical Pearl


Hypomagnesemia is a cofactor for reactions that utilize adenosine triphosphate (ATP). Most importantly, hypomagnesemia therefore causes sodium-potassium-ATPase pump dysfunction, which can lead to dangerous cardiac arrhythmias. You will notice that it is a commonly ordered electrolyte on the wards.




What are the causes of hypokalemia?


Causes of hypokalemia can be classified into four major categories. The first category is a decreased intake of potassium; second is potassium loss via the gastrointestinal tract; third is potassium loss via the renal system; and fourth is a transcellular shift of potassium into cells (see Table 52.1).



It is rare for a healthy individual to develop hypokalemia simply by not eating enough as there is a sufficient amount of potassium in the normal Western diet. However, this is a very common reason for hospitalized patients to develop hypokalemia. Many patients have severe nausea/vomiting and cannot tolerate a regular diet. Other patients are instructed not to eat or drink for a procedure or as a therapeutic modality for an underlying illness (ileus, pancreatitis, etc.). It is also common for postoperative patients not to be able to eat for many days following a surgery. This is why potassium is added to maintenance IV fluids when patients are not able to eat in the hospital. Depending on their condition, patients may need between 40 and 80 mEq of potassium chloride (KCl) a day (which is why you will commonly see patients get about 2 to 3 liters of maintenance fluids per day, with 20 to 40 mEq of KCl added per liter).


Diarrhea is a common cause for relatively minor levels of hypokalemia. It is not a cause of hypokalemia that requires a significant workup to rule in as it is evident from the patient’s history. It is more important to understand that when patients are having diarrhea, it is helpful to keep a close eye on their serum potassium and appropriately replace it. Furthermore, the presence of diarrhea does not itself rule out other causes of hypokalemia, and they should be investigated when clinically indicated.


The definitive workup of potassium losses from the kidneys is complicated and will be discussed later in this chapter. However, the initial step to evaluate whether the kidneys are involved as an etiology for hypokalemia is very simple: A spot urine potassium concentration can be used. If urine potassium is >15 mEq/L, the kidneys are likely playing a role in the patient’s hypokalemia. In a state of hypokalemia, normal functioning kidneys are very good at minimizing renal potassium losses, and this dramatically lowers the urine potassium concentration. Therefore, if the potassium is found at a normal to high concentration in the urine, there is likely something going wrong with the kidneys themselves, and further workup is indicated.


Different physiologic states and medications can cause a transcellular shift of potassium into cells without actually altering the total body potassium. Most commonly, this includes an alkalemic state and beta-2-agonist or insulin administration. Alternatively, an acidemic state or a lack of insulin can cause a transcellular shift of potassium out of the cells. A “normal” serum potassium concretion in this instance can mislead physicians to presume a patient’s total body potassium is relatively normal when in fact a patient can be severely total body potassium depleted.

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Jun 15, 2016 | Posted by in GENERAL & FAMILY MEDICINE | Comments Off on 52 A 45-Year-Old Female With Nausea, Vomiting, and Abdominal Pain

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