A 38 year-old male with unknown medical history is brought to the emergency department by EMS with agitation and bizarre behavior. According to prehospital report, the patient was acting erratically – shouting incomprehensibly in the middle of a busy street with possible associated seizure activity.

On evaluation, the patient was found to be tachycardic, hypertensive, and markedly agitated. Physical examination with a focus on toxidromes was notable for the presence of rotary nystagmus suggestive of hallucinogen including phencyclidine toxicity. The patient required pharmacologic sedation to allow for a broad evaluation of altered mental status.

ED Course

The patient’s workup including core temperature, head imaging and laboratory tests (including AST/ALT, albumin, INR) were unremarkable with the exception of an ammonia level of 142 umol/L (normal range 16-53), slightly elevated CK, and urine toxicology screen with multiple positive agents. Over the course of several hours in the emergency department, the patient’s mental status gradually improved reaching normal level of alertness and orientation with normal neurological examination. He acknowledged PCP use as well as a prior history of seizures (possibly related to ethanol withdrawal) without routine anti-epileptic drug use. He denied known history of liver disease.

The patient’s hyperammonemia was attributed to a hypercatabolic state secondary to phencyclidine-induced agitation with possible seizure. He was discharged with resources for assistance with substance cessation.

An Algorithm for the Differential Diagnosis of Hyperammonemia:

References:

1. Kalra A, Norvell JP. Cause for Confusion: Noncirrhotic Hyperammonemic Encephalopathy. Clin Liver Dis. 2020;15(6):223-227. doi:10.1002/cld.929
2. Mallet M, Weiss N, Thabut D, Rudler M. Why and when to measure ammonemia in cirrhosis? Clin Res Hepatol Gas. 2018;42(6):505-511. doi:10.1016/j.clinre.2018.01.004
3. Hassan AAI, Ibrahim W, Subahi A, Mohamed A. ‘All that glitters is not gold’: when hyperammonaemia is not from hepatic aetiology. Bmj Case Reports. 2017;2017:bcr-2017-219441. doi:10.1136/bcr-2017-219441
4. Odigwe CC, Khatiwada B, Holbrook C, et al. Noncirrhotic Hyperammonemia Causing Relapsing Altered Mental Status. Bayl Univ Medical Cent Proc. 2017;28(4):472-474. doi:10.1080/08998280.2015.11929312
5. Upadhyay R, Bleck TP, Busl KM. Hyperammonemia: What Urea-lly Need to Know: Case Report of Severe Noncirrhotic Hyperammonemic Encephalopathy and Review of the Literature. Case Reports Medicine. 2016;2016:1-10. doi:10.1155/2016/8512721
6. Walker V. Severe hyperammonaemia in adults not explained by liver disease. Ann Clin Biochem. 2011;49(3):214-228. doi:10.1258/acb.2011.011206
7. Laish I, Ari ZB. Noncirrhotic hyperammonaemic encephalopathy. Liver Int. 2011;31(9):1259-1270. doi:10.1111/j.1478-3231.2011.02550.x
8. LaBuzetta JN, Yao JZ, Bourque DL, Zivin J. Adult Nonhepatic Hyperammonemia: A Case Report and Differential Diagnosis. Am J Medicine. 2010;123(10):885-891. doi:10.1016/j.amjmed.2010.02.029
9. Clay AS, Hainline BE. Hyperammonemia in the ICU. Chest. 2007;132(4):1368-1378. doi:10.1378/chest.06-2940
10. Weng T-I, Shih FF-Y, Chen W-J. Unusual causes of hyperammonemia in the ED. Am J Emerg Medicine. 2004;22(2):105-107. doi:10.1016/j.ajem.2003.12.011
11. Hawkes ND, Thomas GAO, Jurewicz A, et al. Non-hepatic hyperammonaemia: an important, potentially reversible cause of encephalopathy. Postgrad Med J. 2001;77(913):717. doi:10.1136/pmj.77.913.717

The post Hyperammonemia appeared first on Differential Diagnosis of.

A 56 year-old male with a history of alcoholic cirrhosis complicated by esophageal varices presents to the emergency department with abdominal distension. He notes gradually worsening symptoms over the past 2 weeks – roughly correlating with the timing of his last paracentesis. He has limited access to medical care and typically presents to emergency departments for palliative paracenteses. He is otherwise in his usual state of health and denies fevers, chills, abdominal pain, vomiting blood, or dark/bloody stools.

Vital signs are notable for a heart rate of 97bpm and blood pressure of 110/65mmHg – otherwise normal. Examination demonstrates a distended abdomen which is non-tender, dull to percussion and with a palpable fluid wave. Bedside ultrasonography shows large, homogenous-appearing ascites with readily-accessible pockets for drainage in the bilateral lower quadrants. A palliative paracentesis is performed with uncomplicated extraction of 4 liters of translucent, straw-colored fluid. Ascitic fluid analysis shows 90 white blood cells of which 10% are polymorphonuclear. The patient is observed briefly in the emergency department, noted symptomatic improvement and was discharged with a plan for telephone follow-up of fluid culture results.

An Algorithm for the Analysis of Ascitic Fluid

References

1. Runyon BA. Care of patients with ascites. N Engl J Med. 1994;330(5):337-342. doi:10.1056/NEJM199402033300508.
2. Wong CL, Holroyd-Leduc J, Thorpe KE, Straus SE. Does this patient have bacterial peritonitis or portal hypertension? How do I perform a paracentesis and analyze the results? JAMA. 2008;299(10):1166-1178. doi:10.1001/jama.299.10.1166.
3. Tarn AC, Lapworth R. Biochemical analysis of ascitic (peritoneal) fluid: what should we measure? Ann Clin Biochem. 2010;47(Pt 5):397-407. doi:10.1258/acb.2010.010048.
4. Li PK-T, Szeto CC, Piraino B, et al. ISPD Peritonitis Recommendations: 2016 Update on Prevention and Treatment. Perit Dial Int. 2016;36(5):481-508. doi:10.3747/pdi.2016.00078.
5. MacIntosh T. Emergency Management of Spontaneous Bacterial Peritonitis – A Clinical Review. Cureus. 2018;10(3):e2253. doi:10.7759/cureus.2253.

The post Ascitic Fluid appeared first on Differential Diagnosis of.

A 43-year-old female with a history of hypertension, diabetes and obesity presents with right-upper quadrant abdominal pain for the past 1 week. The pain is characterized as burning, non-radiating, intermittent (with episodes lasting 10-30 minutes), resolving spontaneously and without apparent provoking features. She notes nausea but no vomiting, no changes in bowel or urinary habits. She similarly denies fevers, chest pain or shortness of breath. Vital signs were normal, and physical examination was notable only for right upper quadrant tenderness to palpation without rigidity or guarding.

An ECG demonstrates normal sinus rhythm, laboratory tests including liver function tests and lipase were normal and a bedside ultrasound of the right upper quadrant was performed demonstrating gallstones and a positive sonographic Murphy sign. The patient was diagnosed with acute cholecystitis, antibiotics were initiated, the patient was maintained NPO while general surgery was consulted.

Evaluation of Right-Upper Quadrant Abdominal Pain

The initial evaluation of a patient presenting with right-upper quadrant (or adjacent) abdominal pain typically includes laboratory tests such as a complete blood count, chemistry panel, liver function tests and serum lipase. In patients at risk for atypical presentations for an acute coronary syndrome or with other concerning symptoms, electrocardiography and cardiac enzymes may be indicated.

The differential diagnosis is broad. A systematic approach proceeds anatomically from superficial to deeper structures centered around the site of maximal pain.

Ultrasound in the Evaluation of Right Upper Quadrant Abdominal Pain

The diagnosis is unlikely to be made based on laboratory tests alone ¹. However, the addition of bedside ultrasound, particularly for the evaluation of gallbladder pathology, is both rapid and reliable ^2-8. The algorithm below provides a pathway for the incorporation of bedside ultrasound of the right upper quadrant in the evaluation of suspected gallbladder disease.

A normal-appearing gallbladder absent gallstones should prompt a traversal of the anatomic approach to the differential diagnosis detailed above. If gallstones are identified, the association with a positive sonographic Murphy sign is highly predictive of acute cholecystitis ^2,5,6,9. Acute cholecystitis may be associated with inflammatory gallbladder changes such as wall-thickening (>3mm) or pericholecystic fluid ^3,5,6,10-13. However, in the absence of cholelithiasis or a positive sonographic Murphy sign, these features are non-specific and may be the result of generalized edematous states such as congestive heart failure, renal failure, or hepatic failure and critically-ill patients may develop acalculous cholecystitis ^7,11,14. Finally, common bile duct dilation may be due to intra-luminal obstruction as in choledocholithiasis, luminal abnormalities such as strictures, or extra-luminal compression from masses or malignancy.  Dilation is generally described as a diameter >6mm – allowing an additional 1mm for every decade over 60 years-old as well as more vague accommodations for patients with prior cholecystectomy ^3,5,7,15.

Gallery

The POCUS Atlas
The ultrasound images and videos used in this post come from The POCUS Atlas, a collaborative collection focusing on rare, exotic and perfectly captured ultrasound images.

Gallstones

Many gallstones

Gallbladder wall thickening

Pericholecystic fluid

Choledocholithiasis

Common bile duct dilation

References

1. Trowbridge RL, Rutkowski NK, Shojania KG. Does this patient have acute cholecystitis? JAMA. 2003;289(1):80-86.
2. Scruggs W, Fox JC, Potts B, et al. Accuracy of ED Bedside Ultrasound for Identification of gallstones: retrospective analysis of 575 studies. West J Emerg Med. 2008;9(1):1-5.
3. Ross M, Brown M, McLaughlin K, et al. Emergency physician-performed ultrasound to diagnose cholelithiasis: a systematic review. Acad Emerg Med. 2011;18(3):227-235. doi:10.1111/j.1553-2712.2011.01012.x.
4. Jang T, Chauhan V, Cundiff C, Kaji AH. Assessment of emergency physician-performed ultrasound in evaluating nonspecific abdominal pain. Am J Emerg Med. 2014;32(5):457-460. doi:10.1016/j.ajem.2014.01.004.
5. Kendall JL, Shimp RJ. Performance and interpretation of focused right upper quadrant ultrasound by emergency physicians. J Emerg Med. 2001;21(1):7-13.
6. Summers SM, Scruggs W, Menchine MD, et al. A prospective evaluation of emergency department bedside ultrasonography for the detection of acute cholecystitis. Ann Emerg Med. 2010;56(2):114-122. doi:10.1016/j.annemergmed.2010.01.014.
7. Rubens DJ. Ultrasound Imaging of the Biliary Tract. Ultrasound Clinics. 2007;2(3):391-413. doi:10.1016/j.cult.2007.08.007.
8. Rosen CL, Brown DF, Chang Y, et al. Ultrasonography by emergency physicians in patients with suspected cholecystitis. American Journal of Emergency Medicine. 2001;19(1):32-36. doi:10.1053/ajem.2001.20028.
9. Shea JA. Revised Estimates of Diagnostic Test Sensitivity and Specificity in Suspected Biliary Tract Disease. Arch Intern Med. 1994;154(22):2573-2581. doi:10.1001/archinte.1994.00420220069008.
10. Miller AH, Pepe PE, Brockman CR, Delaney KA. ED ultrasound in hepatobiliary disease. J Emerg Med. 2006;30(1):69-74. doi:10.1016/j.jemermed.2005.03.017.
11. Shah K, Wolfe RE. Hepatobiliary ultrasound. Emergency Medicine Clinics of NA. 2004;22(3):661–73–viii. doi:10.1016/j.emc.2004.04.015.
12. Matcuk GR, Grant EG, Ralls PW. Ultrasound measurements of the bile ducts and gallbladder: normal ranges and effects of age, sex, cholecystectomy, and pathologic states. Ultrasound Q. 2014;30(1):41-48. doi:10.1097/RUQ.0b013e3182a80c98.
13. Engel JM, Deitch EA, Sikkema W. Gallbladder wall thickness: sonographic accuracy and relation to disease. American Journal of Roentgenology. 1980;134(5):907-909. doi:10.2214/ajr.134.5.907.
14. Gerstenmaier JF, Hoang KN, Gibson RN. Contrast-enhanced ultrasound in gallbladder disease: a pictorial review. Abdom Radiol (NY). 2016;41(8):1640-1652. doi:10.1007/s00261-016-0729-4.
15. Becker BA, Chin E, Mervis E, Anderson CL, Oshita MH, Fox JC. Emergency biliary sonography: utility of common bile duct measurement in the diagnosis of cholecystitis and choledocholithiasis. J Emerg Med. 2014;46(1):54-60. doi:10.1016/j.jemermed.2013.03.024.

The post Hepatobiliary Ultrasound appeared first on Differential Diagnosis of.

A 47-year-old male with no known medical history presents with dysphagia. He reports 3 weeks of symptoms, describing difficulty predominantly with swallowing solid foods which is aided by the concomitant ingestion of liquids. He points to his throat as the area of discomfort, but has not noted any choking or coughing after attempts at swallowing. He occasionally suffers from “heartburn”, describing a burning sensation in his chest provoked by certain foods and was previously prescribed omeprazole which he has not taken for several years. He denies any prior surgeries, tobacco or alcohol use, relevant family history or similar symptoms in the past.

Physical examination was unrevealing, demonstrating a normal neurological examination, normal phonation, normal oropharynx and no appreciable neck masses. The patient was observed to comfortably swallow water.

He was discharged with gastroenterology follow-up and ultimately underwent esophagogastroduodenoscopy which demonstrated narrowing of the distal esophagus suggestive of a peptic stricture. Dilation was deferred in favor of resumption of proton pump inhibitor therapy.

Types of Dysphagia^1,2

Oropharyngeal³

Characterized by difficulty initiating swallowing and accompanied by choking/coughing, nasopharyngeal regurgitation or aspiration.

Involved anatomy: Tongue, muscles of mastication, soft palate (elevation to close nasopharynx), suprahyoid muscles (elevate larynx), epiglottis (occlude airway), cricopharyngeus muscle (release upper esophageal sphincter). Neurological control predominantly coordinated by cranial nerves (V, VII, IX, X, XII)

Esophageal⁴

Delayed after initiating swallowing and characterized by a sensation of food bolus arresting in transit.

Involved anatomy: Skeletal and smooth muscle along the esophagus and lower esophageal sphincter. Neurological control predominantly coordinated by medulla

Important Historical Features^5,6

• Difficulty with liquids suggests motility problem
• Difficulty with solids only or solids progressing to liquids suggests mechanical obstruction
• Identify a history of head and neck surgery or radiation therapy
• Identify a personal or family history of connective tissue disorder (scleroderma, RA, SLE) which may be associated with esophageal dysmotility
• Review home medications (NSAID, bisphosphonate, potassium chloride, ferrous sulfate)
• Immunocompromised patients are at risk for infectious esophagitis (Candida, CMV, HSV) which are generally associated with odynophagia
• A history of heartburn may be associated with reflux-mediated complications such as erosive esophagitis, peptic stricture, and adenocarcinoma of the esophagus
• Young patients are more likely to be affected by eosinophilic esophagitis
• Patient localization of site of obstruction is generally accurate, patients are more accurate at localizing proximal than distal obstructions⁷

Algorithm for the Evaluation of Dysphagia⁸

Management^9-11

Patients who are safely tolerating oral intake can be referred for outpatient gastroenterology evaluation. Admission should be considered for patients at high-risk for aspiration.

References

1. Spieker MR. Evaluating dysphagia. Am Fam Physician. 2000;61(12):3639-3648.
2. Abdel Jalil AA, Katzka DA, Castell DO. Approach to the patient with dysphagia. Am J Med. 2015;128(10):1138.e17-.e23. doi:10.1016/j.amjmed.2015.04.026.
3. Shaker R. Oropharyngeal Dysphagia. Gastroenterol Hepatol (N Y). 2006;2(9):633-634.
4. Galmiche JP, Clouse RE, Bálint A, et al. Functional esophageal disorders. Gastroenterology. 2006;130(5):1459-1465. doi:10.1053/j.gastro.2005.08.060.
5. McCullough GH, Martino R. Clinical Evaluation of Patients with Dysphagia: Importance of History Taking and Physical Exam. In: Manual of Diagnostic and Therapeutic Techniques for Disorders of Deglutition. New York, NY: Springer New York; 2012:11-30. doi:10.1007/978-1-4614-3779-6_2.
6. Cook IJ. Diagnostic evaluation of dysphagia. Nat Clin Pract Gastroenterol Hepatol. 2008;5(7):393-403. doi:10.1038/ncpgasthep1153.
7. Wilcox CM, Alexander LN, Clark WS. Localization of an obstructing esophageal lesion. Is the patient accurate? Dig Dis Sci. 1995;40(10):2192-2196.
8. Trate DM, Parkman HP, Fisher RS. Dysphagia. Evaluation, diagnosis, and treatment. Prim Care. 1996;23(3):417-432.
9. American Gastroenterological Association medical position statement on management of oropharyngeal dysphagia. Gastroenterology. 1999;116(2):452-454. doi:10.1016/S0016-5085(99)70143-5.
10. Spechler SJ. American Gastroenterological Association medical position statement on treatment of patients with dysphagia caused by benign disorders of the distal esophagus. Gastroenterology. 1999;117(1):229-232. doi:10.1016/S0016-5085(99)70572-X.
11. Varadarajulu S, Eloubeidi MA, Patel RS, et al. The yield and the predictors of esophageal pathology when upper endoscopy is used for the initial evaluation of dysphagia. Gastrointest Endosc. 2005;61(7):804-808.

The post Dysphagia appeared first on Differential Diagnosis of.

Young male with no significant medical history presenting with progressively worsening right lower quadrant abdominal pain with marked tenderness to palpation and involuntary guarding.

Imaging

Differentiation between Portal Venous Gas and Pneumobilia

References

1. Rabou Ahmed A and Frank Gaillard. “Pneumobilia.” Radiopaedia. http://radiopaedia.org/articles/pneumobilia.
2. Morgan Matt A and Donna D’Souza. “Portal venous gas.” Radiopaedia. http://radiopaedia.org/articles/portal-venous-gas
3. Sebastià C, Quiroga S, Espin E, Boyé R, Alvarez-Castells A, Armengol M. Portomesenteric vein gas: pathologic mechanisms, CT findings, and prognosis. Radiographics. 2000;20(5):1213–24–discussion1224–6. doi:10.1148/radiographics.20.5.g00se011213.
4. Sherman SC, Tran H. Pneumobilia: benign or life-threatening. J Emerg Med. 2006;30(2):147-153. doi:10.1016/j.jemermed.2005.05.016.

The post Portal Venous Gas appeared first on Differential Diagnosis of.

Key Historical Features

Quantity

Patient’s estimate

Symptoms suggestive of anemia/volume depletion: (pre)syncope, dyspnea

Appearance/Location

Distinguish upper from lower GI bleding

PMH

Prior episodes and source

History of aortic aneurysm graft

Comorbidities: presence of CAD, CHF, liver disease or diabetes increases mortality

Medications/substance use

Gastrotoxic, anti-coagulants, anti-platelet agents

Alcohol abuse

Key Physical Findings

Vital signs

Tachycardia or hypotension

Eyes

Conjuntival pallor suggests anemia

Scleral icterus suggests liver disease

Abdomen

Hyperactive bowel sounds may be present in UGIB (blood is cathartic)

Epigastric tenderness to palpation suggests PUD

Diffuse tenderness suggests bowel ischemia, obstruction/ileus, or perforation

Rectal (digital, anoscopy)

May reveal fissures, hemorrhoids or polyps

Labs/Diagnostic Tests

• CBC: consider transfusion for Hb <8-10g/dL particularly in elderly or those with CAD
• BMP: BUN:creatinine > 36 in the absence of renal failure suggests UGIB
• PT/PTT/INR: coagulopathy
• Lactate: elevated in bowel ischemia or systemic hypoperfusion
• T&S or T&C
• ECG: screen for myocardial ischemia

Blatchford Scoring System

References:

1. Goralnick, E., & Meguerdichian, D. (2013). Gastrointestinal Bleeding. In Rosen's Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 248-253). Elsevier Health Sciences.

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Complications of Nausea and Vomiting

• Hypovolemia: activates RAAS
• Metabolic alkalosis: loss of hydrogen ions in vomitus
• Hypokalemia: RAAS promotes sodium retention and potassium excretion
• Esophageal injury: Mallory-Weiss tear, Boerhaave syndrome
• Aspiration

Key Historical Findings

Duration of vomiting

Acute: Episodic and occurring for <1 week. Suggestive of obstructive, toxic/metabolic, infectious, ischemic or neurologic process.

Chronic: Episodic and occurring for >1 month. Suggestive of partial obstruction, motility disorder or neurologic process.

Onset

Acute onset: suggests pancreatitis, gastroenteritis, or cholecystitis.

Timing

Post prandial: delayed >1 hour suggests gastric outlet obstruction or gastroparesis.

Contents

Bile: presence of bile suggests patent connection between duodenum and stomach (no GOO)

Undigested food: suggests upper GI tract process (achalasia, esophageal stricture, Zenker)

Feculent: suggests distal bowel obstruction

Associated symptoms

Headache: suggests elevated ICP

Causes of Nausea and Vomiting

References

1. Zun, L. (2013). Nausea and Vomiting. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 238-247). Elsevier Health Sciences.

The post Nausea and Vomiting appeared first on Differential Diagnosis of.

1. Visceral: distension of hollow organs or capsular stretch of solid organs.
2. Somatic: parietal peritoneal irritation
3. Referred
   • Extra-abdominopelvic
     • Epigastric: inferior MI
     • Pelvic: hip
     • Abdominal: lower lobe pneumonia/infarction
   • Abdominopelvic
     • Shoulder: diaphragmatic irritation (ex. perforated duodenal ulcer, splenic pathology)
     • Mid-back: aortopathy, pancreatitis
     • Flank: renal pathology
     • Low back: uterus, rectum

Concerning Historical Features

• Elderly: increased probability for severe disease with poor clinical diagnostic accuracy
• Immunocompromised: HIV/AIDS, uncontrolled diabetes, chronic liver disease, chemotherapy, other immunosuppression
• Pain preceding nausea/vomiting: increased likelihood of surgical process
• Abrupt onset, duration <48h, constant timing
• Prior abdominal surgical history: consider bowel obstruction
• No prior episodes of similar pain
• Recent antibiotic or steroid use: may mask signs of infection
• Cardiac risk factors (HTN, vascular disease, atrial fibrillation: increased risk for mesenteric ischemia or aortic aneurysm
• Heavy NSAID use or anticoagulation: increase concern for gastrointestinal bleeding

Imaging

• Plain film reserved for those who would otherwise not undergo CT. XR abdomen for bowel obstruction or radiopaque foreign body.
• CT abdomen/pelvis with IV contrast, particularly if elderly or immunocompromised.
• Ultrasound preferred for hepatobiliary pathology
• Bedside ultrasound for identification of IUP, free intraperitoneal fluid, cholecystitis, CBD dilation, ascites, hydronephrosis, aortopathy, volume status.

Causes of Abdominal Pain

References

1. Budhram, G., & Bengiamin, R. (2013). Abdominal Pain. In Rosen’s Emergency Medicine – Concepts and Clinical Practice (8th ed., Vol. 1, pp. 223-231). Elsevier Health Sciences.

The post Abdominal Pain appeared first on Differential Diagnosis of.

59F with a reported history of congestive heart failure, presenting with intermittent chest discomfort for three days.

She characterized this discomfort as “heartburn”, describing a mid-epigastric burning sensation radiating up her neck, not associated with exertion, lasting 1-2 hours and resolving with antacids. The patient has poor exercise tolerance at baseline and for the past several years has been able to ambulate only short distances around her home, and states that these symptoms have been worsening in the past week. She denies chest pain on exertion, orthopnea or paroxysmal nocturnal dyspnea. She states that she was diagnosed with congestive heart failure five years ago, but was never prescribed medications.

On further questioning, the patient reports several weeks of mouth and lip pain which has limited oral intake, though no dysphagia to solids or liquids. She otherwise denies fevers/chills, abdominal pain, nausea/vomiting, cough, changes in urinary or bowel habits.

In the emergency department, the patient was noted to have an elevated serum troponin, though ECG showed no changes of acute ischemia/infarction.

Physical Exam:

Labs/Studies:

• CBC: 11.1/11.1/34.5/212 (MCV 114.2)
• BMP: 140/4.5/97/20/10/1.14/64
• Anion Gap: 23
• LFT: AST: 73, ALT: 26, AP: 300, TB: 4.6, DB: 2.1, Alb: 3.0, INR 1.3
• BNP: 158
• Troponin: 1.284

Sinus tachycardia, LVH, secondary repolarization abnormalities

Imaging:

CT Pulmonary Angiography:
No evidence of central pulmonary embolism, thoracic aortic dissection, or thoracic aortic aneurysm. Evaluation of the peripheral vessels is limited due to motion artifact. No focal consolidation or pneumothorax.

CT Abdomen/Pelvis non-contrast:
No evidence of intra-abdominal abscess or definite source of infection. Marked hepatic steatosis.

CT Lower Extremity non-contrast:
Diffuse circumferential subcutaneous edema involving both lower extremities from the level of the mid thighs distally through the feet. There are bilateral subcutaneous calcifications which are likely venous calcifications in the setting of chronic venous stasis disease. There is some overlying skin thickening.

TTE:
There is moderate concentric left ventricular hypertrophy with hyperdynamic LV wall motion. The Ejection Fraction estimate is >70%. Grade I/IV (mild) LV diastolic dysfunction. No hemodynamically significant valve abnormalities.

US Abdomen:
Hepatomegaly, echogenic liver suggesting fatty infiltration. Moderately blunted hepatic vein waveforms suggesting decreased hepatic parenchymal compliance.

Assessment/Plan:

The patient was admitted to the cardiology service for management of NSTEMI and evaluation of undiagnosed CHF. She was started on a heparin continuous infusion. In addition, a CT pulmonary angiogram was obtained to evaluate for pulmonary embolism as an explanation of her progressive dyspnea on exertion. No PE, consolidation or effusion was identified.

Despite the patient’s reported history of congestive heart failure, there was no evidence that her symptoms were a result of an acute exacerbation with only a mildly elevated BNP but no jugular venous distension or evidence of pulmonary edema. The patient’s significant lower extremity edema was more suggestive of chronic venous stasis.

One notable laboratory abnormality that was explored was her elevated anion gap metabolic acidosis. Studies submitted included serum lactate, salicylates, osmolarity, CK, and urinalysis for ketonuria. This evaluation was notable for an elevated serum lactate of 13.2mmol/L and an arterial blood gas that showed adequate respiratory compensation (and no A-a gradient). Given the patient’s modest leukocytosis (with neutrophil predominance), and tachycardia, the concern for sepsis was increased though the source remained unclear. Prominent possibilities included a skin and soft-tissue infection vs. less likely intra-abdominal source though the patient’s physical examination was not suggestive of a process that would produce such a substantial lactic acidosis. Blood cultures were drawn and the patient was started on empiric antibiotics for the suspected sources. In addition, the patient was cautiously volume resuscitated given her reported history of CHF while pending a transthoracic echocardiogram to evaluate cardiac function. Additional imaging including CT abdomen/pelvis and lower extremities was obtained (though without contrast due to the patient’s recent exposure), and no obvious source was identified.

Over the next two days, the patient’s serum lactate downtrended to normal range, as did the serum troponin. A transthoracic echocardiogram showed an LVEF >70% with mild concentric hypertrophy and diastolic dysfunction. Blood and urine cultures were without growth.

Additional issues managed during the hospitalization included elevated serum transaminases (AST > ALT), conjugated hyperbilirubinemia and evidence of decreased hepatic synthetic function with hypoalbuminemia and elevated INR. Given the patient’s history of EtOH use, as well as other corroborating findings including macrocytic anemia, hypomagnesemia, folate and B12 deficiency, this was attributed to alcoholic hepatitis (discriminant function <32). Infectious hepatitis serologies were negative. The patient was started on nutritional supplements. Finally, the patient persistently complained of lip and oral mucosal pain. Examination was without discrete lesions but some mucosal redness was identified. Despite poor dentition, there was no evidence of abscess and HSV/HIV testing was negative. This was thought to be stomatitis caused by her identified nutritional deficiencies.

Differential Diagnosis of Elevated Serum Lactate ^1,2

Algorithm for Evaluation of Acidemia ^3,4

Algorithm for Evaluation of Alkalemia ^3,4

References:

1. Fall, P. J., & Szerlip, H. M. (2005). Lactic acidosis: from sour milk to septic shock. Journal of intensive care medicine, 20(5), 255–271. doi:10.1177/0885066605278644
2. Luft, F. C. (2001). Lactic acidosis update for critical care clinicians. Journal of the American Society of Nephrology : JASN, 12 Suppl 17, S15–9.
3. Ingelfinger, J. R., Berend, K., de Vries, A. P. J., & Gans, R. O. B. (2014). Physiological Approach to Assessment of Acid–Base Disturbances. The New England journal of medicine, 371(15), 1434–1445. doi:10.1056/NEJMra1003327
4. Ingelfinger, J. R., & Seifter, J. L. (2014). Integration of Acid–Base and Electrolyte Disorders. The New England journal of medicine, 371(19), 1821–1831. doi:10.1056/NEJMra1215672

The post Lactic Acidosis appeared first on Differential Diagnosis of.

Ultrasound

CT Abdomen/Pelvis

Differential Diagnosis of Biliary Duct Dilation: ^1,2,3

References:

1. Kim, H. J., Lee, K. T., Kim, S. H., Lee, J. K., Lim, J. H., Paik, S. W., & Rhee, J. C. (2003). Differential diagnosis of intrahepatic bile duct dilatation without demonstrable mass on ultrasonography or CT: benign versus malignancy. Journal of gastroenterology and hepatology, 18(11), 1287–1292.
2. Levy, A. D. (2009). Biliary Ducts – Pathology. The Radiology Assistant, 1–4. Retrieved from http://www.radiologyassistant.nl/en/p49e17de25294d/biliary-ducts-pathology.html
3. Teefey, S. A., Baron, R. L., Schulte, S. J., Patten, R. M., & Molloy, M. H. (1992). Patterns of intrahepatic bile duct dilatation at CT: correlation with obstructive disease processes. Radiology, 182(1), 139–142. doi:10.1148/radiology.182.1.1727277

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