United States

Background
Hemorrhage of the adrenal glands is uncommon and can present with a variety of symptoms. A high index of suspicion based on awareness of risk factors associated with the condition is vital as the condition’s mortality rate is estimated at 15%. 

Case Presentation
CH is a 43-year-old male with past medical history of lupus anticoagulant disorder who presented to his PCP with muscle aches, abdominal pain, confusion, poor appetite and tachycardia. One week prior, he had a deep tissue massage where the therapist walked on his back. He also switched from Coumadin to Xarelto approximately one month ago. Two days prior to presenting to his primary care office, he was discharged from the hospital after being admitted with symptoms of back pain, abdominal pain, constipation and dark urine. A CT during that admission revealed a right-sided adrenal hemorrhage. However, with normalization of his urine color and improvement of his abdominal pain following constipation treatments, he was discharged home. At his PCP’s office, a CMP was ordered that revealed a serum Na level of 120 mg/dl. This result cued his readmission. Further workup revealed elevated ACTH and undetectable serum cortisol levels supporting adrenal insufficiency. He was started on IV normal saline and a hydrocortisone regimen. His symptoms gradually improved, and two days later his serum Na was 132 mg/dl. He was then discharged home with a hydrocortisone taper and a follow-up with endocrinology.

Discussion
Risk factors for adrenal hemorrhage include physical trauma, anticoagulants, hypercoagulable states and severe stressors. Anticoagulants are implicated in one third of patients with adrenal hemorrhage. Additionally, it has been found that there is an increased incidence of hemorrhage within the first weeks of initiating anticoagulants. Imaging of the adrenals, particularly CT of the abdomen, can confirm the diagnosis of adrenal hemorrhage. Serum sodium, ACTH and cortisol levels are also vital to obtain as they provide valuable insight on the presence of adrenal insufficiency. Results supporting the diagnosis of adrenal hemorrhage with adrenal insufficiency should prompt treatment with surgical intervention and/or non-invasive management with glucocorticoids as appropriate. These treatments could be lifesaving.


AMA Research Challenge 2022

A Deep Tissue Massage and a Factor Xa Inhibitor: The Recipe for a Life-Threatening Crisis?

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Ricardo Correa, MD, EdD
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Jessica Li, MD/PhD Candidate
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Charles Lopresto, DO

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Welcome to the largest national, multi-specialty research event featuring research from 750 medical students, residents and fellows, and international medical graduates.


Abstract Title:
Flatbush diabetes – ketosis prone atypical diabetes mellitus: A case report

Background:
Flatbush diabetes, also termed as atypical or Ketosis-prone type 2 diabetes mellitus is being increasingly reported. It is characterized by sudden onset ketoacidosis, absence of pancreatic beta cell autoimmunity and dysfunction. Though cases commonly seen amongst African-Americans and Afro-Caribbean individuals, it is also seen in Indian populations. The aetiology is unknown but predisposition to glucose desensitization is suspected.
These patients are typically obese, middle-aged men who has strong family history of type 2 diabetes. Here we report an atypical case of Flatbush diabetes in a young female patient who has no family H/O DM.



Case Presentation:
A 31-year-old female presented to emergency room with complaints of grade IV dyspnea, abdominal distension and 5 episodes of bilious vomiting’s since morning. She has history of recurrent diffuse abdominal pain, vomiting’s, polyuria, polydipsia, weight loss, hair loss for 3 months. Her vitals at presentation are 110/80 mmHg of BP, pulse rate is 122/min and oxygen saturation is 99% on room air.
On examination she is diaphoretic, with severe tachypnea. Capillary blood glucose levels are high (>599). ABG showed PH of 6.99, pCO2 of 7 with no derived values of bicarbonate. urine ketones tested positive with dip stick (3+). She is immediately started on IV fluids and subsequently managed as DKA according to protocols. Her HbA1C is 12%. Her C-peptide levels are with in normal limits. Autoantibodies against GAD, tyrosine phosphatase, insulin are absent. CECT is normal. No family H/O diabetes. She is put on glargine U-100 along with ADA’s and is reviewed after 2 weeks. In these two weeks she didn’t have hypoglycemic attacks and symptoms of DKA, and Urine ketones tested negative. Insulin dose is adjusted and reviewed after 1 month.



Discussion:
This case report sheds light on the atypicality of presentation and summarizes the main diagnostic features of Flatbush diabetes. Absence of autoantibodies to GAD, insulin, tyrosine phosphatase and presence of normal levels of C-peptide rules out type 1 DM. 

This condition may improve after temporary insulin therapy and many patients become insulin-independent eventually. Increased awareness of this atypical form of DM can facilitate early diagnosis and management.



Flatbush diabetes – ketosis prone atypical diabetes mellitus: A case report

Idiopathic Granulomatous Hypophysitis : A Rare Cause of Hypopituitarism

This review analyzes the potential effectiveness of dietary intervention in the management of Polycystic Ovarian Syndrome (PCOS), as well as its associated symptoms and comorbidities. The dietary regimens covered in this review are as follows: the Mediterranean Diet (MD), the Ketogenic Diet (KD), and nutritional therapy utilizing the addition of micronutrients and/or macronutrient distribution manipulation. This review surveys whether effective use of these measures can not only be used as an effective treatment for PCOS but also can assist with its symptoms and comorbidities while limiting drug and surgical regimens.

A literature analysis of English-written, peer-reviewed research through PubMed was conducted to gather evidence on the potential effectiveness of a dietary intervention on PCOS management.

Women who followed a MD were less likely to suffer from PCOS symptoms and lead a healthier lifestyle. This treatment often prevented weight gain, promoted exercise, and decreased the likelihood of development and/or persistence of comorbidities. Additionally, our team gathered significant evidence that the administration of omega-3 fatty acids, folic acid, selenium, vitamin E, catechin, glycyrrhizin, and coenzyme Q10 assists PCOS women, and effectively manages symptoms. 

It can be concluded that the MD allows women to manage and reduce the physical symptoms and comorbidities associated with PCOS most effectively. Firstly, the MD is associated with decreased inflammation, improved hormonal regulation, as well as downregulation of cellular and humoral immunological pathways related to disease activity and progression in PCOS. Although the KD may be beneficial because it reduces carbohydrates leading to improved liver function and insulin sensitivity in PCOS patients, more investigation is required. Additionally, supplementation with omega-3 fatty acids, folic acid, selenium, vitamin E, catechin, glycyrrhizin, and coenzyme Q10 should be considered in women with PCOS. Research indicates that this type of micronutrient supplementation with PCOS patients improves inflammatory factors, biomarkers of oxidative stress, and metabolic parameters. Lastly, diet modification and exercise prevent the onset of metabolic syndrome and infertility in women, specifically in those who follow a low protein and high fiber diet. This can be achieved on a MD, further suggesting the potential benefits of its adoption among the PCOS population.


The Effectiveness of Dietary Intervention on Polycystic Ovarian Syndrome Management: An Exploratory Literature Review

Background: Thyroid storm is a rare condition but life threatening. Having a high index of suspicion is required especially in patients without previous diagnosis of hyperthyroidism. The increasing use of contrasted iodine studies has caused a resurgence of iodine induced hyperthyroidism which in the most severe cases presents as thyroid storm.
Case Presentation: A 21-year-old female presented with 4 weeks of worsening dyspnea. Associated symptoms included abdominal pain, nausea, vomiting and fever. 3 weeks prior to presentation she underwent CT angiogram of the chest which was negative for pulmonary embolism. She had no past medical history and denied any current medications or recreational drugs. Temperature was 98.4 F, heart rate 107 bpm and blood pressure 125/110. On exam she seemed agitated and anxious. Mild exophthalmos, hyperdynamic precordium, tachycardia, and bilateral pedal edema were also present on exam. Labs showed initial TSH 0.00 uIU/mL, elevated free T4 5.3ng/dL and elevated thyroid receptor antibodies. Pregnancy test was negative. She was diagnosed with thyroid storm and treatment initiated with propranolol, hydrocortisone, methimazole and potassium iodide. Later symptoms improved and she was discharged on propranolol and methimazole with plan to follow-up with Endocrinology.
Discussion: Thyroid storm has multisystem involvement which can mimic other conditions such as sepsis leading to delayed diagnosis. Correct diagnosis requires a complete history and physical examination. Use of the Burch-Wartofsky scale is helpful to support diagnosis of thyroid storm; in the case the Burch-Wartofsky score was 40 suggestive of thyroid storm. Looking for precipitating factors is important. These precipitating factors include infection, myocardial infarction, pregnancy, trauma, and large loads of exogenous iodine (contrast or medications like amiodarone). The phenomenon of hypersecretion of thyroid hormone by autonomous areas within the thyroid gland after an acute iodine load is known as the Jod-Basedow phenomenon. It usually develops within 2 weeks of the iodine load. In patients with symptoms suggestive of thyrotoxicosis, exam findings such as thyromegaly/thyroid bruit, or iodine deficiency, it is suggested to request thyroid hormone assay before an iodine contrasted study. 



The Perfect Storm: Thyrotoxic Crisis Precipitated by Iodinated Contrast

Abstract Title:Bleeding from Jejunal Diverticula
Background: Small intestinal hemorrhage is a common location of obscure GI bleeding and can be difficult to diagnose and treat given the limitations of traditional gastroscopes and colonoscopes. Jejunal diverticulosis is very rare with the prevalence of 0.3-1.9% in studies of the small bowel and 0.3-1.3% in autopsy studies. The presentation varies from being asymptomatic to causing massive gastrointestinal hemorrhage. We present a case of massive obscure GI bleeding from jejunal diverticulosis that was able to be successfully treated by deep enteroscopy with a pediatric colonoscope.

Case Presentation: 68-year-old female with PMH of internal hemorrhoids, osteoporosis admitted with 3-day history of dark tarry stool, mild epigastric pain, and associated dizziness. She had no significant GI history.
On admission, she was hemodynamically stable. Exam showed melena. Her Hg was 6.5 gm/dL. She was started on IV PPI and received 2 units of PRBCs. Esophagogastroduodenoscopy was performed that showed a 2mm non-bleeding ulcer in the gastric antrum, thought to be the source of bleeding, but no longer active. She was discharged home on oral PPI as Hb was stable
Three days later, she returned to the ED with continued evidence of ongoing blood loss with multiple episodes of melena. Admission Hg was 6.0mg/dL. After initial PRBC transfusion and preparation, colonoscopy was performed that showed pan-diverticulosis, but no active bleeding. Deep intubation of the terminal ileum showed fresh blood, but no active source could be identified, indicating the source was in the proximal small bowel. 
Enteroscopy was then performed with a pediatric colonoscope that showed multiple jejunal diverticula. A visible vessel with active bleeding was seen within a jejunal diverticulum. Hemostasis was successful with clips and hemostatic powder

Discussion: Jejunal diverticulosis is rare and can be congenital or acquired. Prevalence increases with age and most commonly presents in the 6th and 7th decade. The etiology is unclear, but possibly due to small bowel dysmotility with increased intraluminal pressure. It is often asymptomatic but can cause severe complications including hemorrhage, perforation, enterolith formation, small bowel diverticulitis and intestinal obstruction.
Deep enteroscopy should be considered in patients with suspected small bowel bleeding. 



Bleeding from Jejunal Diverticula

Background: Clinical Cases involving ingestion of foreign bodies are very prevalent in the hospital. While most ingested foreign bodies pass spontaneously, sharp objects could become impacted and cause bowel perforation. Upper endoscopy is an established method for retrieving sharp objects in the esophagus. However, when foreign bodies are located beyond the reach of upper endoscope, management becomes ambiguous with limited studies to demonstrate the safety of sharp object removal with colonoscopy. We hereby report a case in which an ingested foreign object adjacent to appendix was successfully retrieved using colonoscopy

Case presentation: A 39 yo/F presented to the ED with RLQ abdominal pain after swallowing the ball portion of her tongue piercing. On examination, abdomen was soft but tender to palpation in the RLQ. No rebound, guarding or signs of peritonitis. CT of the abdomen and pelvis without contrast revealed 1 cm round metallic object in the RLQ without any signs of perforation. Abdominal x ray revealed a round metallic foreign body in the RLQ and benign bowel gas pattern. Colonoscope was advanced to the right colon. Circular, nonimpacted metallic object was located adjacent to the appendix. Circular metallic object was extracted with the assistance of the Roth net retriever. Colonic mucosa was otherwise normal. Patient was observed and subsequently discharged from the hospital without adverse events

Conclusion: This case further demonstrates the effectiveness of colonoscopy in removing foreign bodies from the colon


Endoscopic Retrieval of an Accidentally Ingested Foreign Body

IL-17A plays a significant role in the autoimmune process of Psoriasis. Ixekizumab, a
humanized IgG4 monoclonal antibody inhibits the interaction between the IL-17A and IL-17 receptor, ultimately neutralizing the cytokines and reducing the inflammation in Psoriasis. It is used for other inflammatory diseases like ankylosing spondylitis, non-radiographic axial spondyloarthritis, plaque psoriasis, and psoriatic arthritis. With the increasing use of this medication, we are experiencing a relevant increase in the number of cases of new-onset IBD and IBD exacerbations. So far, no clear association has been shown in the medical literature between Ixekizumab and IBD, and with our compelling case, we want our audience to be aware of this rare association. A 70-year-old female with a past medical history of psoriatic arthritis was started on Ixekizumab 4 weeks ago and presented with a complaint of diarrhea ongoing for three weeks; she had 15-20 bloody stools every day along with abdominal cramping. Diagnostic studies came positive for FIT, ESR 90, CRP 20.13, and CT imaging showed moderate segment mural thickening with peri-colonic fat stranding in the lower descending colon, sigmoid colon, and rectum, indicating either infectious versus inflammatory colitis. GI and ID were consulted, and she underwent a flexible sigmoidoscopy with intestinal biopsies. Biopsies results did not show any infectious causes and were more consistent with inflammatory bowel disease colitis attributed to her recent Ixekizumab usage. The patient responded well to the intravenous methylprednisolone. Discussion IBD is expected to appear in patients with Psoriasis due to the shared genetic causes of these diseases. Biopsies from patients with IBD show higher expression of the IL-17 protein. Patients with Psoriasis have subclinical IBD, which might be unmasked with Ixekizumab by an imbalance caused by the blockade of the IL-17A and the IL-17 receptor. All patients with previously diagnosed IBD should be counseled about this association. Before starting Ixekizumab in psoriatic patients, it is essential to evaluate the gastrointestinal symptoms and specific inflammatory markers like fecal calprotectin. These factors should be monitored to identify early warning signs of the illness and prevent severe complications.

Ixekizumab Causing Inflammatory Bowel Disease

We present the case of a young patient going into hemorrhagic shock due to gastroepiploic artery bleeding after laparoscopic sleeve gastrectomy. Patient was resuscitated and taken back to OR for controlling bleed.

Massive Gastroepiploic Artery Bleed Causing Hemorrhagic Shock After Sleeve Gastrectomy: A Case Report

Background
Mauriac Syndrome is a unique complication of prolonged periods of poor glycemic control in children and adolescents with Type 1 Diabetes Mellitus. Patients present with hepatomegaly secondary to glycogen deposits in the liver. Subsequent hormonal axis disruptions cause short stature and delayed puberty.

Case Presentation
A 15-year-old male with a history of Type 1 Diabetes Mellitus, Celiac Disease, and Growth Hormone Deficiency presented to the Emergency Department with a 5-month history of worsening abdominal pain and distention. He denied fever, weight loss, loss of appetite, emesis, constipation or diarrhea.
Pertinent physical exam findings included generalized abdominal tenderness and hepatomegaly palpable 5 cm below the right costal margin. Weight and height were below the 1st percentile.
Lab findings included Hgb A1c 10.1%, elevated AST 743, ALT 969, Alk Phos 420, GGT 927, Glucose 586, Anion Gap 23.2, UA 4+ glucose/1+ ketones, POC Gas pH 7.3, and HCO3 16.9. Following a normal saline bolus and subcutaneous insulin, his glucose improved to 277, pH 7.4, and HCO3 25.
Imaging revealed an enlarged liver shadow on abdominal x-ray. Ultrasound and MRI of the abdomen confirmed hepatomegaly without masses. Bone Age scan revealed borderline delayed bone age.
He was admitted to the inpatient floor. Endocrinology coordinated his insulin regimen with significant improvement of his hyperglycemia and transaminitis.

Discussion
Mauriac Syndrome should be considered in a pediatric patient with diabetes presenting with hepatomegaly, growth/puberty delay, and short stature. Achieving adequate glycemic control and optimizing an insulin regimen is key to management. With treatment, hepatomegaly resolves, however, growth delays are not easily reversed. Patient education on glucose management and consistent Endocrinology follow up is critical to prevent the development of Mauriac syndrome.

Mauriac Syndrome: Glycogen Hepatopathy in a Pediatric Patient

We describe an immunocompromised individual with chronic diarrhea who developed an acute kidney injury in the setting of chronic Norovirus infection.

A 75 year-old female with cadaveric renal transplant 10 years prior (on immunosuppression) presented with acute right flank pain, worsening fatigue and unintentional weight loss of 80 lbs for over a year. She was tachycardic and hypotensive with a non-tender right lower quadrant renal transplant. Laboratories showed a bicarbonate of 12 mEq/L, blood urea nitrogen of 35 mg/dL, creatinine of 2.4 mg/dL (baseline creatinine 0.9) and white blood cell count of 4.4 K/mcL. Urine studies showed 3+ protein and protein/creatinine ratio of 7,900 mg/g. Tacrolimus level was appropriate. A renal transplant ultrasound was nonspecific, revealing mildly elevated resistive indices measuring 0.8-0.9 suggestive of transplant dysfunction. Serology for Epstein-Barr virus and Cytomegalovirus was negative. Renal biopsy was obtained and was not consistent with either rejection or polyomavirus nephropathy. Patient reported episodes of watery diarrhea. Over the past year, she had painless intermittent diarrhea often requiring hospitalization. A positive stool viral PCR for Norovirus from 6 months ago was discovered on hospital records. Stool studies of C. difficile, Legionella, Shigella, Campylobacter, Salmonella, Cryptosporidium/Cyclospora and Giardia were negative and positive for Norovirus. She was treated with oral immunoglobulin (IG) with a decrease in diarrhea. Her creatinine improved to 1.3.

Norovirus infection may progress to chronic infection after a solid organ transplant. Generally self-limiting, norovirus infection in immunocompromised individuals can lead to prolonged symptoms and viral shedding for many years. Minimal information is available in terms of prevalence of chronic Norovirus infection among solid organ transplant recipients. One study showed a prevalence of 4.6% among solid organ recipients. Of these, 22.8% developed chronic infection, with a median shedding period of 218 days. Currently, there are no approved human antiviral agents that are effective against Norovirus. Treatment using oral IG was extrapolated from its role in management of primary immunodeficiency conditions. In our patient, viral shedding continued but oral IG provided symptomatic relief, decreasing the progression of kidney injury. Physicians should be made aware of this particular presentation and treatment options in renal transplant patients.


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