This morning, Jerry Lipinski, one of our stellar R2s presented an interesting patient he recently took care of at the VA: a 53-year-old woman with a history of Rheumatoid Arthritis who presented with acute bloody diarrhea. Her initial presentation was notable for sinus tachycardia, LLQ tenderness, leukocytosis. We used the opportunity to work through our differential diagnosis and discuss the work-up to obtain.
A CT scan of the abdomen showed non-specific inflammation of the colon in the splenic flexure and adjacent bowel. We highlighted some of the common findings on imaging – mucosal thickening, edema, fat stranding, and “thumbprinting” (haustra of the large bowel becoming thickened and projecting into the intestinal lumen at regular intervals). The patient then underwent colonoscopy which showed patchy erythematous, edematous, and friable mucosa consistent with ischemic colitis. We were very lucky to have Dr. Cynthia Hsu, an alumnus of our residency and current GI fellow as a discussant to walk us through the findings.
We then talked about the causes of ischemic colitis, which can broadly be divided into occlusive and non-occlusive etiologies. We also discussed one common reason to have ischemia in “watershed” areas of the colon – episodic hypoperfusion. The exact cause of ischemic colitis in any given patient is often difficult to find, and in this case, there was reason to suspect that the patient’s TNF-alpha inhibitor (adalimumab) for RA was the culprit. This adverse event has been described in the literature for biologic agents. Additionally, the patient had been transitioned from etanercept to adalimumab two years prior due to colitis that at the time was not further specified.
Our surgical colleagues were consulted, but the patient did not require intervention and improved over several days of conservative management. She was treated for 5-day course of antibiotics – the routine use of antibiotics is not necessary, but this patient’s clinical status was concerning (rising leukocytosis and extensive colonic involvement on endoscopy) that the team needed to treat potential bacterial gut translocation.
A special thank you to Dr Hsu for all her high-yield clinical pearls!
This morning we were lucky to be joined by Dr. Judd Landsberg, one of our stellar VA Pulmonary professors, for a discussion of the management of pneumothoraces. We discussed the pathophysiology of how air enters and is trapped within the pleural space and causes progressive lung collapse. We then moved on to the first management issue of pneumothorax – conservative management with supplemental oxygen versus placement of a chest tube. We discussed the difference between placing a chest tube to “suction” versus “water seal,” as well as how to troubleshoot tubing malfunctions. We also discussed two interventional options (Video Assisted Thorascopic Surgery and Endobronchial Valve Placement) for patients whose pneumothorax increases on water seal. Finally, we discussed how to assess when a chest tube is ready to be removed (resolution of the PTX along with an absence of air leak).
A special thank you to Dr. Landsberg for sharing his wisdom and approach to pneumothorax management with us. Check out his diagrams and schemas – just a teaser of the high-yield content available in his manual which is based on his experiences caring for our vets!
On Thursday morning at the VA, we discussed the management of acute COPD exacerbation. The patient was a 65 year-old man with GOLD class D COPD admitted several hours prior with increased productive cough and wheezing for the past 5 days. He developed worsening shortness of breath with evidence of diffuse wheezing and accessory muscle use on physical exam despite treatment with antibiotics, bronchodilators, and corticosteroids. His labs were consistent with an acute on chronic respiratory acidosis and the decision was made to initiate bi-level non-invasive ventilation. With the help of our expert pulmonologist, Dr. Mark Fuster, we discussed the variables to consider when initiating BiPAP as well as how to interpret the machine interface and waveforms.
We then discussed variable that indicate that hypercarbic respiratory failure is responding to NIV, and the need to remain at bedside to assess the patient in real time. An hour later, the patient continued to be tachypneic with evidence of worsening acidosis. We considered variables to troubleshoot, including assessment of tidal volumes, adequacy of EPAP, and evaluation of patient-ventilator dyssynchrony (including the need to watch out for dynamic hyperinflation!) The patient in this case had a large amount of leak around his face mask (due to a full beard) and improved when switched to a nasal interface and an increase in his driving pressure.
Special thanks to Dr. Fuster and all our participating residents!
We’re continuing to practice our clinical skills with a daily ECG! Today’s diagnosis: acute pericarditis. Two aspects of the ECG point to this diagnosis:
Diffuse ST elevations (leads I, II, III, aVF, V3-V6) indicated by arrows. In myocardial infarction the ST elevations tend to be localized (inferior, anterior, posterior, lateral), often with reciprocal ST depressions.
PR segment displacement indicated by asterisks. PR elevation can be seen in aVR and PR depression are seen in leads II, aVF, V4-V6.
This morning we welcomed Dr. Dena Rifkin, nephrologist extraordinaire, to discuss the limitations of serum creatinine and the use of Cystatin C as an alternative for the estimation of renal function. We started by considering a 59-year-old man that presented to primary care clinic to discuss an elevated Cr to 1.43 (eGFR of 46). There was no clear sign of personal risk factors for CKD, although he occasionally used Ibuprofen and had a family history of Type II Diabetes and Hypertension. He had no microalbuminuria and his Cr was stable compared to three years prior. We obtained a Cystatin C level that indicated an eGFR of 82.
We then discussed why serum creatinine needs to be interpreted within the context of the patient’s physiology and how estimation calculators (including the preferred CKD-EPI equation) make adjustments for age, race, and sex. Cystatin C is an alternate biomarker produced by all nucleated cells that is freely filtered by glomeruli that avoids those problematic corrections. Cystatin C allows for increased detection of GFR reductions in the “creatinine blind range” where large changes in GFR are not reflected by substantial changes in GFR. Caution needs to be exercised when using Cystatin C in inflammatory states (infection, malignancy) and obesity as those will create higher levels of the protein. We then went through three patient cases that demonstrate the discrepancy in eGFR when using serum Cr versus CysC.
Cystatin C is available with rapid turnaround times at both the VA and UCSD – use it today!
Thursday morning, Brian Coburn, one of amazing second year Med/Peds residents, presented an interesting case of a 35-year-old patient who presented with hypoactive delirium. The patient’s medical history was significant for epilepsy and opioid use disorder. We started our investigation of possible causes of the patient’s encephalopathy by going through the AEIOUTIPS mnemonic of common causes of altered mental status that can be investigated with basic history, exam, labs, and imaging. Our expert discussants from the Toxicology services provided us a comprehensive overview of the approach to hypoactive toxidromes and judicious interpretation of urine tox screening. After the initial work-up was unrevealing, the team pursued additional investigation with lumbar puncture, EEG, and MRI without contrast that were also negative. The team asked our friends from psychiatry to help elucidate whether the patient’s symptoms may be due to an underlying psychiatric disorder, but the determination was made that a primary medical disease was still the most likely cause.
The patient’s condition continued to progress, and an MRI with contrast ultimately revealed acute, diffuse white matter lesions. Per our radiology colleagues, the differential for these findings included infection/post-infectious causes (viral encephalitis, acute disseminated encephalomyelitis, acute hemorrhagic leukoencephalitis), autoimmune encephalitis, and toxic leukoencephalopathy. Following a repeat LP that was negative for a broad array of infectious, autoimmune, and malignant/paraneoplastic studies, we were left with a diagnosis of opiate-induced toxic leukoencephalopathy. The disease presentation is extremely variable, ranging from minor cognitive impairment, easily confused with psychiatric illnesses, to severe neurological dysfunction. Our toxicologist reminded us that some of these findings can also be seen with potential transient, out-of-hospital anoxic episodes. While there is no proven treatment for toxic leukoencephalopathy, antioxidant therapy with Coenzyme Q10, Vitamin E, and Vitamin C has been used to treat some patients with variable results in the past. The patient received this treatment and spontaneously improved after several days of therapy.
Thank you to Brian, our expert discussants, and our residents for working through the differential of hypoactive delirium and the sequential investigations we needed to get to the bottom of this fascinating case.
Tuesday morning report at the VA was all about diuretics. We presented a case of a 73-year-old man with history of CHF, CKD and T2DM who presented with progressive dyspnea, bilateral lower extremity swelling, orthopnea, and abdominal distension. Physical exam showed evidence of volume overload with 3+ pitting edema, elevated JVD, and bibasilar pulmonary crackles. We considered various common triggers of heart failure exacerbation before diving into a discussion of diuretics.
Key points that we highlighted:
Decongestion with resolution of symptoms and edema is achieved through “diuresis” = loss of sodium (natriuresis) + loss of water (diuresis). That is why sodium-limited diet is crucial in treatment of fluid overload.
Loop diuretics function as “threshold” drugs that need to achieve a sufficient concentration in order to work. The natriuretic threshold is higher in patients with acute CHF than in healthy persons. That is why hospitalized patients require loop diuretic doses that are higher than stable outpatient doses.
Loop diuretics exhibit a “ceiling” effect and doses above the ceiling will not increase the amount of natriuresis. Acute CHF shifts the relation between plasma diuretic concentration and sodium excretion to the right and reduces the “ceiling.”
Patients with chronic diuretic use develop post-diuretic sodium retention and decreased efficacy with each subsequent loop diuretic dose. That is why loop diuretics are dosed multiple times daily and why patients need a net negative sodium balance each day.
Chronic loop diuretic use leads to distal tubular hypertrophy and once maximum loop diuretic effect is reached, auxiliary diuretics are sometimes used (thiazide, aldosterone antagonists, carbonic anhydrase inhibitors). We discussed specific situations you may consider using these agents.
Ethacrynic acid is the loop diuretic of choice in patients with sulfa allergy.
For further reading, check out this review from the NEJM:
Ellison DH, Felker GM. Diuretic Treatment in Heart Failure. N Engl J Med. 2017 Nov 16;377(20):1964-1975.
At Hillcrest this morning Janna Raphelson, one of our stellar residents, presented a case of a 75-year-old man with history of steroid-dependent interstitial lung disease, chronic kidney disease, and serious TMP-SMX allergy who presented to the VA with increased dyspnea, fatigue, and headache one month after starting dapsone for Pneumocystis jiroveci pneumonia prophylaxis. He was found to have an acute anemia that was stabilized by transfusion of pRBCs and subsequently characterized as hemolytic. On exam, the patient was cyanotic with an oxygen saturation in the mid-80% that was unresponsive to up titration of supplemental oxygen.
We were joined by Dr. Mark Hepokoski from our PCCM division as we unpacked the causes of hypoxemia and why we need to calculate an alveolar-arterial (A-a) gradient. While the patient’s A-a gradient was increased (from baseline IPF and mild interstitial edema), there was a clear discrepancy between his SpO2 (pulse oximeter) and PaO2 (blood gas). This reminded us that impaired oxygen delivery to tissues (hypoxia) has multiple potential etiologies: hypoxemic, anemic, circulatory, histotoxic. The next step in the evaluation of our patient involved obtaining co-oximetry which revealed increased levels of methemoglobin!
The pulse oximeter is only able to distinguish between saturated and unsaturated hemoglobin. If significant levels to methemoglobin build up, the machine interprets this as a saturation of approximately 85%. In addition to causing a functional anemia, methemoglobinemia shifts the hemoglobin-oxygen dissociation curve to the left. This effect causes increased affinity of hemoglobin for oxygen and decreases oxygen unloading in tissues. We compared our patient’s case to the other acquired dyshemoglobinemia that we sometimes encounter, carbon monoxide poisoning.
Despite the patient’s normal G6PD screen prior to starting dapsone, he still developed known complications of this medication’s oxidative effect: hemolytic anemia and methemoglobinemia. Our patient’s methemoglobinemia was partially treated by blood transfusions and given concern for toxicity in renal failure, he did not receive the standard treatment of methylene blue and vitamin C. The patient slowly recovered following discontinuation of dapsone (switched for inhaled pentamidine for ongoing PJP ppx) and is now back to his baseline.
Thank you to Dr. Hepokoski for sharing his wisdom and clinical expertise and thank you to all of our applicants for joining us for another great morning report!
This Thursday, we restarted our join teaching conferences with our partners in Maputo, Mozambique! We discussed a case of an 83-year-old man who presented with several months of progressive shortness of breath, dry cough, and weight loss. On exam, he had absence of breath sounds over the right hemithorax with dullness to percussion and absent tactile fremitus. His chest radiograph demonstrated unilateral white out, and we considered two possibilities for this finding: a large pleural effusion or a mainstem bronchial obstruction causing lung collapse.
Our expert discussant, the legendary VA pulmonologist Dr. Judd Landsberg, guided us through the CXR interpretation and why it was consistent with an effusion: large spacing between ribs and tracheal deviation away from the affected hemithorax.
A thoracentesis was performed and was consistent with an exudate by Light’s criteria. We formed a differential for exudative effusion and discussed why two possibilities were most likely for this particular patient: malignancy and Tuberculosis. Unfortunately, the patient’s thoracentesis was followed by the discovery of a pneumothorax. We considered the mechanism and management of this complication and how to proceed in case where the pneumothorax is increasing: placement of a chest tube.
Thank you to Dr. Landsberg for all of his clinical pearls and the Maputo residents for their participation!
This morning we were lucky to be joined by Dr. Darcy Wooten, an amazing HIV Medicine attending and APD of the Infectious Disease Fellowship, to discuss one of her Owen clinic patients.
The 30-year old man with newly diagnosed HIV presented to our hospital with cough, fevers, chills, night sweats, decreased appetite, and recent weight loss. On admission, the patient had a CD4 count of 102 cell/uL and viral load of 185,000 copies/mL. The CXR revealed a diffuse micronodular/miliary pattern and CT showed upper lobe predominant diffuse ground glass opacities. Initially concerning for TB, the patient’s work-up was significant for elevated serum Coccidiodes IgG antibodies, positive cocci complement fixation with a 1:512 titer, and negative bone scan and spine computerized tomography. The patient was diagnosed with severe pulmonary coccidioidomycosis with presumed dissemination (based on the high titer).
The patient was treated with amphotericin B for severe cocci and discharged on fluconazole therapy (along with antiretroviral therapy and Bactrim prophylaxis). He could not tolerate the fluconazole and was switched to Posaconazole. The patient subsequently developed severe hypertension refractive to amlodipine, lisinopril, and hydrochlorothiazide. Work up demonstrated low levels of potassium, renin, and aldosterone. The patient was diagnosed with pseudohyperaldosteronism, taken off Posaconazole, and placed on itraconazole and spironolactone, leading to a resolution side effects. The mechanism behind pseudohyperaldosteronism is similar to that of licorice root extract, where steroid synthesis products directly activate mineralocorticoid receptors. Treatment is focused on cessation of Posaconazole and antagonism of the mineralocorticoid receptor with spironolactone.