SOAP Note Case Study
Mr. L is a 42-year-old man with type 1 diabetes mellitus (DM) who complains of weakness, anorexia, abdominal pain, and vomiting. Laboratory studies demonstrate a HCO3− of 6 mEq/L.

Mr. L reports that he has had diabetes since he was 10 years old. His diabetes has been complicated by peripheral vascular disease requiring a below the knee amputation and laser surgeries for retinopathy. Two days ago, he began experiencing nausea and some vomiting. He continued to take his insulin. Physical exam reveals supine BP of 90/50 mm Hg and pulse of 100 bpm. Upon standing, his vital signs are BP, 60/30 mm Hg; pulse, 150 bpm; RR, 24 breaths per minute; and temperature, 37.0°C. Retinal exam reveals dot-blot hemorrhages and multiple laser scars. Lungs are clear to percussion and auscultation. Cardiac exam reveals a regular rate and rhythm with a grade I/VI systolic murmur at the upper left sternal border. Abdominal exam is soft and nontender. Stool is guaiac-negative. Lab studies reveal Na+, 138 mEq/L; K+, 6.2 mEq/L; HCO3−, 6 mEq/L; Cl−, 100 mEq/L; BUN, 40 mg/dL; creatinine, 1.8 mg/dL; glucose, 389 mg/dL; WBC, 10,500/mcL; HCT, 42%; ALT (SGPT), AST (SGOT), and lipase are normal.

ABG: pH of 7.15, PaO₂ of 80 mm Hg, and PaCO₂ of 20 mm Hg.

The low pH confirms that the primary disorder is an acidosis.

HCO₃⁻ = 6 mEq/L and PaCO₂ = 20 mm Hg.

Both the HCO₃⁻ and PaCO₂ are low. Since only a low HCO₃⁻ would create an acidosis the primary disorder is a metabolic acidosis. (A low PaCO₂ drives the pH up [see above].)

Anion gap = 138 − (6 + 100) = 32 (Normal = 12 ± 4)

Clearly, the primary disorder is an anion gap metabolic acidosis. By referring to Table 4-1, the differential diagnosis can be narrowed to the remaining possibilities of diabetic ketoacidosis (DKA), other ketoacidoses, lactic acidosis, uremia, or toxin.

Mr. L’s serum ketones are large. He denies any history of heavy alcohol use or abuse. The serum lactate level is 1 mEq/L (normal 0.5–1.5 mEq/L).

Mr. L confirms he has been taking his insulin. He reports no fever, rigors, dysuria, cough, shortness of breath, diarrhea, or abdominal pain. Urinalysis, chest radiograph, and lipase were sent to search for the precipitating event. All of the results were normal. An ECG revealed T wave inversion in leads V1–V4, suggesting anterior myocardial ischemia. Troponin T levels were elevated consistent with an acute MI (believed to be the precipitant of his DKA). He was transferred to the ICU for monitoring. He received fluid resuscitation, IV insulin until his ketoacidosis resolved, and supplemental potassium (when his potassium fell below 5.3 mEq/L). His MI was treated with beta-blockers and aspirin. Subsequent cardiac catheterization revealed triple vessel disease. After stabilization, he underwent coronary artery bypass grafting and did well.

SOAP Note 

Diabetic Ketoacidosis occurs when the body produces high levels of ketones. In Mr. L’s case, after careful evaluation of the diagnostic exams and his history of DM 1, we find the differential diagnosis to be DKA. As per the text, DKA often begins with an acute illness, including MI, which was noted in Mr. L. Additionally, Mr. L presented with almost every symptom associated with DKA both specific and nonspecific including nausea, vomiting, weakness and abdominal pain. More significantly, Mr. L’s orthostatic changes notate profound dehydration and hypotension, which help us to differentiate our diagnoses. It is important when evaluating an acid-base sickness to utilize a step-wise approach to determine the particular disorder. Utilizing the step-wise approach allows practitioners to make thoughtful and accurate diagnoses. With this case, the use of this approach allowed the practitioner to confidently rule out uremic acidosis, alcoholic acidosis or starvation acidosis due to the diagnostic findings.  Uremic acidosis is unlikely with mild renal insufficiency; alcoholic ketoacidosis is ruled out by the fact that Mr. L denies heavily drinking and starvation ketoacidosis is ruled out with the high glucose levels found in the blood. With an ABG of 7.15, the primary disorder is an acidosis and with an HCO3- of < 24 mEq/L and equal to 6 mEq/L, it is safe to assume the primary disorder is metabolic acidosis and not respiratory as the PaCO2 is equal to 20 mmHg and <40 mmHg (sign of respiratory acidosis). Mr. L’s anion gap is elevated at 32 and suggests the presence of anion gap metabolic acidosis, which is the diagnoses found in his case. Ketoacidosis occurs most often in patients with an insulin deficiency (i.e. DM 1) and with criteria all similar to those produced in Mr. L’s case. It is important to note the precipitant is the most frequent cause of mortality in DKA, and the large role that the particular precipitant has on causing DKA. In the case of DKA, one of the precipitants is a myocardial infarction, which we see in Mr. L’s case, among others including infection, discontinuation of insulin, new onset type 1 DM, CVA, PE and drugs. The summation of Mr. L’s complaints, the diagnostic results obtained and studies performed allow the practitioner to confidently diagnose Mr. L with DKA s/p MI.

Reflection
In my case assignment for Unit 3, I covered a case on Acid-Base chemistry. It was very interesting to me to see the science of acid-bases be put in to practice from a medical perspective. In our AMS class, we are also covering acid-base disorders and the diagnostic parallels between what was seen in the case and what we’re learning in the classroom are astounding. It’s been interesting to see the material we’re covering across our courses intertwine over the past few weeks (and I suspect that was done on purpose). For me, being able to learn something and then apply it in a medical setting has been very rewarding and served as a means to keep working hard. The case discussed the step-wise approach practitioners should take in evaluating a patient with suspected DKA. Similarly in evaluating the Acid-Base problems in AMS, we were also instructed to take a 5-step approach to ensure we’re diagnosing the correct disease and to determine whether or not it was compensated or uncompensated. The step-wise approach in acid-base cases helps practitioners to make a sound diagnosis in practice. This case was my first experience with writing a SOAP note and for me, was a great way to ease into the process. Previously, as a scribe, I have written hundreds of Emergency Room notes but the SOAP note was a different take for me. Typically the patient is moved out of the ED and there is no progress report or follow up needed after that transfer. That approach forced me to look at the story from a different perspective and to ensure I’m providing only what is accurate and relevant to a provider who may read the patient’s chart after I’ve left for the day. As we continue to expand our knowledge, I suspect my SOAP note writing skills will become stronger and I will be able to handle without the aide of the details provided in the text, and I look forward to that point in my studies.

Diagnosing DKA

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