Differential Diagnosis and Hospital Course History Physical Exam And
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Sudden Onset Altered Mental Status Anees Daud, MD Intermountain Medical Center History Differential Diagnosis and Hospital Discussion A 71-yr-old woman with a past significant history of relapsing- Course Serotonin syndrome is characterized by a clinical triad of mental remitting multiple sclerosis, anxiety, and depression, presented to status changes, autonomic hyperactivity, and neuromuscular the emergency department with a one day history of altered mental abnormality. There is a significant amount of variability in the Initial diagnostic work up was targeted towards her history of status. The patient’s husband and granddaughter provided the presenting symptoms. These can range from mild symptoms, multiple sclerosis and presence of a possible occult infection. history. The patient was reportedly in her usual state of health until which include akathisia and tremors, to severe symptoms, which She was started on broad spectrum antibiotics (vancomycin and 9AM on the day of presentation, when she began to act “strangely” include clonus, muscular hypertonicity, and hyperthermia (>40C) zosyn) since infection was highest on the differential. The and “confused.” The patient was altered in the ED as well, at one (Figure 2). The pathophysiology of serotonin syndrome is based negative MRI and absent inflammatory cells in the CSF made point taking off her clothes and walking around the ED. on the hyper-activation of serotonergic neurons. In the central active multiple sclerosis very unlikely. Infectious nervous system, they belong in the midline raphe nuclei which meningitis/encephalitis was also unlikely based on those results. Of note, the patient had recently been under significant stress are located in the brainstem from the midbrain to the medulla. In Blood/urine culture/CSF cultures were negative for bacteria, because one of her daughters was going through a divorce and had the CNS, serotonergic neurons are responsible for wakefulness, fungi, HSV, and VZV. moved in with her parents. Her medications included norco, affective behavior, thermoregulation, and motor tone. In the PNS, duloxetine, bupropion, donepezil, pregabalin, levothyroxine, these neurons are responsible for regulation of vascular tone and Since there was no improvement within the first 12-24hrs, other omeprazole, fosamax, docusate, and occasional zolpidem. gastrointestinal motility. This helps to explain the clinical findings diagnoses were explored. Further history from the husband in patients suffering from this syndrome. revealed that with the recent onset of home stressors, the patient had perhaps been taking higher doses of some of her The diagnosis of Serotonin medications. Syndrome is based entirely Physical Exam and Diagnostic Studies on clinical criteria (Figure After reevaluation of her history and clinical presentation, 3). My patient met the The patient’ s vital signs were T 36.2C, BP 187/80, HR 116, RR 22, specifically her tremors, hyperreflexia, inducible clonus, agitation, criteria based on the and SaO2 90% on room air. On exam, she was agitated, impulsive, and diaphoresis, a diagnosis of Serotonin Syndrome was made. presence of tremor and attempting to climb out of bed, and unable to carry on a Since the patient’s home serotonergic medications were already hyperreflexia, and the conversation. She was diffusely tremulous, especially in the upper held on admission, she required only supportive management for presence of inducible extremities. She was diaphoretic, and skin was warm to the touch. her autonomic instability and agitation. This was managed clonus, agitation, and Cranial nerves were difficult to test, but she had appropriate lateral primarily with hydralazine, lorazepam, and haloperidol, diaphoresis. The EOMs, and no facial asymmetry. She had hyperreflexia in the biceps, respectively. The patient’s mental status returned to baseline management consists of triceps, and patellar tendons. Two to three beats of ankle clonus within the next three days, and she was discharged with removal of the offending improved clinical status and with home health physical therapy to agents, and supportive were present. She was tachycardic with a regular rhythm. Chest was Figure 3. clear to auscultation. Abdomen was soft, but tender diffusely, and recover from deconditioning. care. bowel sounds were active. The agitation can be controlled with benzodiazepines, which Initial labs showed WBC 8.5K/uL (47.4% PMNs, 41.7% lymphs, 6% blunts the hyperadrenergic state (mortality benefits have been monos, 3.4% eos, 1.1% baso), Hg 14.4 g/dL, and Plt 302K/uL. The shown in animals). For severe cases (extreme hyperthermia, CMP was unremarkable, as were the TSH, lipase, hepatitis panel, muscular hypertonicity), management may include sedation, and ESR/CRP. The urinalysis did not show evidence of a UTI, and neuromuscular paralysis, and intubation to prevent urine toxicology screen showed synthetic opioids. Lactic acid was rhabdomyolysis. elevated at 3.7. Blood and urine cultures were obtained in the ED. EKG showed sinus tachycardia with a significant amount of Figure 1. movement artifact (Figure 1). References A chest x-ray and CT abdomen/pelvis were unremarkable. The ED 1.Boyer, EW, Shannon, M. The Serotonin Syndrome. N Engl J Med. consulted Neurology, who recommended an MRI brain/spine. This 2005;352:1112-20. did not show any acute processes or new multiple sclerosis lesions. 2.Mason PJ, Morris VA, Balcezak TJ. Serotonin syndrome. Lumbar puncture had normal protein and glucose, and was negative Presentation of 2 cases and review of the literature. Medicine for WBCs and bacteria/fungi on gram stain. (Baltimore) 2000; 79:201. Figure 2. Images courtesy of Intermountain Medical Center Takotsubo Cardiomyopathy: A Case Report Ashley R. Donaldson, MD Intermountain Medical Center History Differential Diagnosis/Hospital Course Discussion A 78 year old female with a history of diabetes mellitus, chronic The differential diagnosis for this patient’s presentation of epigastric Takotsubo cardiomyopathy is a relatively rare event, although its kidney disease and chronic urinary tract infections presented to the pain wth dyspnea included acute coronary syndrome, pnemonia, incidence has increased in recent years. It is commonly triggered by Emergency Department via EMS following two episodes of takotsubo cardiomyopathy, and gastroesophageal reflux disease. one of three inciting factors including iatrogenic causes, neurologic hypoglycemia. On the night prior to admission, the patient’s son had Given the concern for a cardiac event she was started on ACS events, and emotional or physical stressors. Iatrogenic causes are difficulty awakening her. He checked her blood glucose, which was protocol. numerous, including sympathomimetic, alpha adrenergic, 40. An amp of dextrose administered by EMS improved her glucose anticholinergic, and para-sympatholytic medications. Similarly, to 113 and she remained at home the rest of the evening. Over the course of admission her neurologic events that cause catecholamine release and sympathetic (3) At 5:00 the morning of admission the patient was again difficult to troponin and activation have been associated with takotsubo. All of these factors arouse. In the ED her blood glucose was 26. She was given another CK-MB levels can cause an increase in catecholamine levels. The apex of the amp of dextrose; her blood glucose increased to 120. Three hours continued to rise, myocardium has a greater vulnerability to sudden surges in later she was again hypoglycemic with a blood glucose of 21. peaking at 2.11 catecholamine levels and thus results in the hypokinesis noted on (3) Following dextrose she was started on a D5W infusion. and 5.2, perfusion scans of takotsubo patients. Emotional/physical stressors are common in the general population, but few patients develop The patient reported starting glimepiride 3 months prior. She denied respectively, 24 takotsubo, thus indicating predisposing factors also play a role. any history of hypoglycemic events but did endorse experiencing a hours after initial “panic attack” one month earlier while getting a CT scan. She stated onset. Chest x- Risk factors for takotsubo cardiomyopathy are categorized into this episode felt similar to a hypoglycemic event, with racing of her Figure 1. ECG with left bundle branch block. ray showed no cardiovascular (HTN, smoking, HLD, CAD), associated co- heart, dizziness and lightheadedness. significant morbidities (endocrinopathies, malignancy), and endothelial cardiopulmonary dysfunction, (atherosclerosis, systemic inflammatory disorders, The morning after admission the patient complained of epigastric abnormality (Figure 2). Transthoracic echocardiography results estrogen deficiency).(2) The diagnosis is most common in post- pain and shortness of breath. Her pain was similar to that of showed an ejection fraction of 33%, segmental wall motion menopausal females, likely because of the decreased estrogen state, as heartburn. She stated both of these symptoms were new but felt abnormalities, a severely hypokinetic/akinetic right ventricular apex, estrogen protects against myocardial damage during similar to her prior panic attack. She also reported heart palpitations, and tricuspid regurgitation. Myocardial PET perfusion scan was ischemia/reperfusion through induction of endothelial nitric oxide fevers, and chills, but denied substernal chest pain, pain radiating to Conclusions subsequently performed, demonstrating a small, fixed apical defect synthase. her back, nausea or vomiting.