Severe Metabolic Acidosis: A Case of Triple Hit with Ketogenic Diet, Vinegar, and Metformin in an Obese Patient.

Obesity is an epidemic with high burden of disease. It is directly proportional to increased risk of morbidity and mortality. Ketogenic diet and herbal supplements have recently gained popularity amongst patients struggling with weight loss. There are limited data available for most of these supplements contrary to the claims laid by the mainstream media. Due to lack of awareness, this patient population is at high risk of adverse effects. We present a case of severe acidosis secondary to ketogenic diet and acetic acid (vinegar) ingestion. The use of dietary acetic acid is usually well tolerated; however, in this case, the large quantities and presence of acute renal injury may have worsened the acidosis. Severe ketosis in setting of ketogenic diets is a serious complication, which is infrequently reported in literature. Many of these diets and supplements may seem harmless, but as our case illustrates, when combined with other risk factors, patients can face adverse effects and even hospitalization. It is imperative that such dietary practices are physician supervised to avoid complications. With the recent surge of over-the-counter weight loss supplements and fat diets, physicians need to engage in dietary discussion with patients when attempting to lose weight.

Rasburicase induced severe hemolysis and methemoglobinemia in a Caucasian patient complicated by acute renal failure and ARDS.

Rasburicase is a recombinant urate-oxidase enzyme and is a very important medication for tumor lysis syndrome. Methemoglobinemia and hemolysis are known side effects of rasburicase that result from oxidative stress caused by hydrogen peroxide, a byproduct generated during the breakdown of uric acid to allantoin. Patients with G6PD deficiency have a decreased tolerance to oxidative stress and are therefore at a greater risk of hemolysis and methemoglobinemia with rasburicase. Our patient is a 56-year-old Caucasian male with a recent diagnosis of grade 2-3a non-Hodgkin's lymphoma who presented to our emergency department with shortness of breath and dark discoloration of urine. Patient was discharged 36 hours ago from our hospital after he was given a first course of R-CHOP regimen and a dose of rasburicase. On further evaluation, patient was found to have severe anemia with hemolytic picture, hyperkalemia and acute kidney injury. He also had a discrepancy of the transcutaneous saturation (75%) and the saturation in an arterial blood gas value (99%). His methemoglobin level was found to be 11.9%. We were aware that methylene blue is a contraindication in patients with G6PD deficiency but considering patient being Caucasian and low risk for it and his deteriorating respiratory condition, it was decided to offer the treatment and patient received 1 dose of methylene blue which failed to improve his methemoglobinemia. He was also given vitamin C and 8 units of packed red blood cell throughout his stay in the hospital. Patient's hospital course was complicated by ARDS needed to be on mechanical ventilation support for 4 days and acute renal failure secondary to pigment nephropathy and acute tubular necrosis which required a hemodialysis support. Even if rasburicase induced methemoglobinemia and hemolysis are not very common complications, clinicians who prescribe and follow patients should detect this serious complication early and manage it accordingly. Our case can be used as a reminder that patients should be followed closely and given the right instructions on discharge to treat these complications which are associated with severe consequences. It is also vital to assume a diagnosis of G6PD deficiency until proven otherwise in a patient who presents with rasburicase induced hemolysis and avoid administration of methylene blue even if the patient is from a low risk ethnicity for G6PD as in our patient.

Kounis syndrome secondary to gadolinium contrast agent.

Cases of coronary artery spasm secondary to contrast agent use are rarely reported. Herein, we report the case of a 53-year-old woman who developed chest pain, dyspnea, and bradycardia and quickly become unresponsive after magnetic resonance imaging of the brain. A heart monitor showed ST elevation, and an electrocardiogram showed ST elevations in leads II, III, aVF, V3, and V4 and ST segment depression in lead I. Urgent left heart catheterization revealed no evidence of obstructive coronary artery disease or pulmonary embolism. A few days later, she was discharged from the hospital with no symptoms. A type I variant of Kounis syndrome was diagnosed.

Pulmonary vein thrombosis secondary to tuberculosis in a non-HIV infected patient.

Our patient is a 67-year-old male with a past medical history significant for hypertension and hyperlipidemia came to a hospital with hemoptysis. He was also having cough and shortness of breath for the last 1 month. He said that his hemoptysis was about 1 cup per day mixed with yellowish sputum. He noticed around 20 pounds of weight loss in the last 1 month. He also complained of night sweats but had no fever. He had no history of travel outside the USA. He has never been incarcerated before, but he endorsed that his son has been to Jail before and he visited him twice a year in patient's home. But he also said that his son has never been diagnosed with TB. He smoked 1.5 packs per day for the last 50 years and quit smoking 2 months ago. His medication include hydrochlorothiazide, lisinopril, gabapentin, aspirin and trazodone. On examination, vital signs were within the normal range except a hearty rate of 106 beats/minute. He had slightly pale conjunctiva, non-icteric sclera and had wet tongue and buccal mucosa. There was decreased air entry with crepitations in the right side of the posterior chest but no wheezes or rales. No peripheral lymphadenopathy, no peripheral edema or sign of fluid collection in the abdomen. Chest x ray showed multiple cavitary lesion in the right upper lobe area. CT scan of the chest with PE protocol showed pulmonary venous partial thrombosis in the right upper lobe. Multiple cavitary lesions with hilar and mediastinal lymphadenopathy. There are also smaller nodular lesions in the left chest too. Small right pleural effusion with multiple calcified granulomata in the left upper lobe. QuantiFERON gold test was found to be positive. Sputum AFB smear was found to be strongly positive and it is sensitive to rifampin. Echocardiography showed no valvular lesions with preserved ejection fraction (>65%) and normal right ventricular size and normal right ventricular systolic pressure. Liver enzymes and renal function tests were found within the normal limit. HIV test was negative. Patient was started with intensive phase anti-tuberculosis treatment with rifampin, isoniazid, ethambutol, pyrazinamide with vitamin B6. He was also started with anticoagulation with heparin and warfarin considering the tuberculosis being the cause of the pulmonary vein thrombosis. Patient was also given supportive treatment and he made a gradual improvement and was discharged with anti-tuberculosis treatment and warfarin. Patient needed to be placed on a higher dose of warfarin as it was difficult to keep him therapeutic with lower doses. He was also advised to follow with infectious disease and anticoagulation clinic. Patient was found to have a significant increase in liver enzymes and bilirubin on follow up and the anti-TB medications were stopped to be restarted one by one with a follow up of his liver enzymes and liver function tests. He was also continued with warfarin.