Tissue Isn’t the Issue

Journal of Hospital Medicine 13(7). 2018 July;:500-504. Published online first April 25, 2018 | 10.12788/jhm.2963

April 25, 2018|Journal of Hospital Medicine

Lekshmi Santhosh, MD;Laura Koth, MD;Thomas E. Baudendistel, MD;Bradley Sharpe, MD;Bradley Monash, MD

The approach to clinical conundrums by an expert clinician is revealed through the presentation of an actual patient’s case in an approach typical of a morning report. Similar to patient care, sequential pieces of information are provided to the clinician, who is unfamiliar with the case. The focus is on the thought processes of both the clinical team caring for the patient and the discussant.

A 43-year-old man with a history of asplenia, hepatitis C, and nephrolithiasis reported right-flank pain. He described severe, sharp pain that came in waves and radiated to the right groin, associated with nausea and nonbloody emesis. He noted “pink urine” but no dysuria. He had 4prior similar episodes during which he had passed kidney stones, although stone analysis had never been performed. He denied having fevers or chills.

The patient had been involved in a remote motor vehicle accident complicated by splenic laceration, for which he underwent splenectomy. He was appropriately immunized. The patient also suffered from bipolar affective disorder and untreated chronic hepatitis C infection with no evidence of cirrhosis. He smoked one pack of tobacco per day for the last 10 years and reported distant alcohol and methamphetamine use.

Right-flank pain can arise from conditions affecting the lower thorax (effusion, pneumonia, pulmonary embolism), abdomen (hepatobiliary or intestinal disease), retroperitoneum (hemorrhage or infection), musculoskeletal system, peripheral nerves (herpes zoster), or the genitourinary system (pyelonephritis). Pain radiating to the groin, discolored urine (suggesting hematuria), and history of kidney stones increase the likelihood of renal colic from nephrolithiasis.

Less commonly, flank pain and hematuria may present as initial symptoms of renal cell carcinoma, renal infarction, or aortic dissection. The patient’s immunosuppression from asplenia and active injection drug use could predispose him to septic emboli to his kidneys. Prior trauma causing aortic injury could predispose himto subsequent dissection.

The patient appeared well with a heart rate of 100 beats per minute, blood pressure 122/76 mmHg, temperature 36.8°C, respiratory rate 16 breaths per minute, and oxygen saturation 96% on room air. His cardiopulmonary and abdominal examinations were normal, and he had no costovertebral angle tenderness. His skin was warm and dry without rashes. His white blood cell (WBC) count was 26,000/μL; absolute neutrophil count was 22,000/μL. Serum chemistries were normal, including creatinine 0.63 mg/dL, calcium 8.8 mg/dL, and phosphorus 3.1 mg/dL. Lactate was 0.8 mmol/L (reference range: 0-2.0 mmol/L). Urinalysis revealed large ketones, >50 red blood cells (RBC) per high power field (HPF), <5 WBC per HPF, 1+ calcium oxalate crystals and pH 6.0. A bedside ultrasound showed mild right hydronephrosis. Computed tomography (CT) with intravenous contrast of his abdomen and pelvis demonstrated diffuse, mildly prominent subcentimeter mesenteric lymphadenopathy and no kidney stones. He was treated with intravenous fluids and pain control, and was discharged with a presumptive diagnosis of a passed kidney stone.

A passed stone would not explain this degree of leukocytosis. The CT results reduce the likelihood of a renal neoplasm, renal infarction, or pyelonephritis. Mesenteric lymphadenopathy is nonspecific, but it may signal underlying infection or malignancy with spread to lymph nodes, or it may be part of a systemic disorder causing generalized lymphadenopathy. Malignant causes of mesenteric lymphadenopathy (with no apparent primary tumor) include testicular cancer, lymphoma, and primary urogenital neoplasms.

His flank pain resolved over the next few days. One week later, he presented with fevers, diffuse headache, painful oral ulcers, pain in the knees and ankles, and a rash involving the face, trunk, and extremities. He was febrile to 38.1°C, normotensive, with an oxygen saturation of 96% on room air. He had erythema and swelling of the right eyelid and upper orbit, 2 shallow oral ulcers on the lower buccal mucosa, and bilateral, firm, nontender, 1-cm cervical lymphadenopathy. His visual acuity was normal. His bilateral ankles and knees were warm and tender with small effusions but preserved range of motion. He had innumerable scattered erythematous papules with rare pustules, interspersed with large, erythematous plaques on his face, extremities, back, and buttocks with a predilection for previous scars and tattoos (Figure 1). He also had tender, erythematous nodules on his anterior lower extremities. His neurological exam was normal.

The lower extremity nodules are consistent with erythema nodosum, which may be observed in numerous infectious and noninfectious illnesses. The rapid tempo of this febrile illness mandates early consideration of infection. Splenectomized patients are at risk for overwhelming post-splenectomy infection from encapsulated organisms, although this risk is significantly mitigated with appropriate immunization. The patient is at risk of bacterial endocarditis, which could explain his fevers and polyarthritis, although plaques, pustules, and oral ulcers would be unusual. Disseminated gonococcal infection causes fevers, oral lesions, polyarthritis and pustular skin lesions, but plaques are uncommon. Disseminated mycobacterial and fungal infections may cause oral ulcers, but affected patients tend to be severely ill and have profound immunosuppression. Secondary syphilis may account for many of the findings; however, oral ulcers would be unusual, and the rash tends to be more widespread, with a predilection for the palms and soles. Human immunodeficiency virus (HIV) can cause oral ulcers and is the chief viral etiology to consider.

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