Today we reviewed a case of a middle aged gentleman with a long history of alcoholism who presented with diffuse abdominal pain and rectal bleeding and was found to have a direct bilirubin of nearly 30. We first went through the differential for direct hyperbilirubinemia, which can be placed in two broad categories, intrahepatic cholestasis & obstruction.
We reviewed the clinical manifestations of alcoholic hepatitis and were reminded that it is typically a patient with long-standing alcoholism who presents with jaundice, abdominal pain, direct hyperbilirubinemia, an AST:ALT typically ~300 or less in a 2:1 pattern, low albumin and sometimes fever/leukocytosis and no infectious etiology.
The diagnosis is a clinical one, and remember..obstruction must be considered. Infection is commonly present initially but can also develop later and one must also be hypervigilant about infection. We discussed the discriminant function score, which estimates the severity of alcoholic hepatitis once the diagnosis is made – a score of >32 predicts a high risk of mortality and steroid therapy may be useful. We reviewed the data briefly and made a case that it is uncertain whether it is useful, but it is certainly harmful in cases in which steroids are contraindicated, such as infection, active GIB, uncontrolled hyperglycemia, acute pancreatitis and psychosis.
If you and your team decide to use steroids, check a Lille Score at 7 days to determine if steroids are helping, and if you complete a 28 day course, make sure to taper the steroids afterwards.
As our GI fellow stated, what clearly shows a mortality benefit is alcohol cessation…use their admission as an opportunity to counsel them! The remainder of care is supportive, and should include attention to volume status, electrolyte repletion (remember K, Mg, Phos), nutrition (enteral preferred), and monitoring for the usual complications of cirrhosis. Lastly, nonselective beta blockers should be temporarily held in patients with severe AH until it resolves as it increases the risk of acute kidney injury.
We went through a case of an elderly gentleman who presented with productive cough, shortness of breath, leukocytosis, and a large left pleural effusion.
In the evaluation of a pleural effusion in the setting of a suspected pneumonia, pleural fluid sampling is imperative. Parapneumonic effusion is an umbrella term for any type of pleural effusion in the setting of an adjacent pneumonia and can be divided into uncomplicated/simple and complicated effusions.
Uncomplicated effusions are usually small (i.e. costophrenic angle blunting, <10mm on lateral decubitus radiograph, or estimated volume <100mL). If they are sampled, they do not contain evidence of infection (negative gram stain/culture, normal glucose, and pH >7.2). These do not require treatment separate from treatment of the underlying pneumonia. However, they can become infected and if clinical improvement is not observed in 2-4 days, repeat imaging should be performed to check if the effusion has increased in size.
Complicated effusions are any effusions that are infected, including empyemas (pus within the pleural cavity). Typical features of a complicated pleural effusion include loculations, large size (>0.5 hemithorax), thickened pleura, split pleura sign on CT, and sepsis. These effusions have exudative features upon pleural fluid sampling, high WBC count (usually neutrophilic if bacterial), pH <7.2, and glucose <60. They should be promptly treated with antibiotics with coverage of anaerobes as well as Strep species, usually a 3rd generation cephalosporin with Flagyl OR Augmentin. Drainage should also be attempted as soon as possible with chest tube placement.
It was previously thought that large bore chest tubes were the treatment of choice, but according to the MIST1 trial, smaller catheters had much improved pain scores without worse outcomes, although they did have more frequent blockages, which can be alleviated by sterile saline flushes Q6h.
Today we learned about a very uncommon mechanical complication after MI to a patient with subacute pleuritic pain and dyspnea and found to have an inferior MI on EKG. A TTE was concerning for an aneurysm and a left heart cath revealed a large aneurysm on the LV-gram.
We reviewed the common complications after MI (arrhythmia and heart failure) as well as the three major mechanical complications after MI (all of which are exceptionally rare). They all can occur 0-14 days after MI. We did not discuss, Dressler syndrome, which can occur a few weeks to even a year after MI and is fever
Ventricular Septal Defect
- presents as a holosytolic murmur along left sternal border, often with a thrill
- EKG findings are non-specific
- TTE reveals a high velocity L->R shunt
Papillary Muscle Rupture
- presents as a holosytolic murmur along left sternal border and apex;
- EKG findings are usually associated with inferior/inferior-posterior wall MI
- TTE reveals a flail leaflet with severe mitral regurgitation
LV Free Wall Rupture
- presents as hypotension, JVD, distant heart sounds
- EKG findings are non-specific
- TTE reveals a pericardial effusion with tamponade, discrete wall motion abnormality; a defect in the myocardium can sometimes be seen
- if the rupture is incomplete and contained within the pericardium, this can cause a pseudoaneurysm and is highly prone to rupture. surgical intervention is the treatment of choice
We presented a fascinating case of a middle aged woman who presented with fatigue, weakness, and a significant weight loss in the past year who was found to have hypotension refractory to a usual fluid challenge. Her AM cortisol was low and her post-stim cortisol remained <18, confirming the diagnosis of adrenal insufficiency. Her ACTH was inappropriately on the low end of normal, consistent with a central AI (secondary or tertiary). Here are the highlights:
Clinical Manifestations in Primary AI only:
- Generalized hyperpigmentation of the skin and mucus membranes (exclusively in chronic primary adrenal insufficiency)
- Hyponatremia/hyperkalemia and hypoglycemia generally occurs in primary AI only
Diagnosing Adrenal Insufficiency
- An AM cortisol < 3 is sufficient, but a ACTH stimulation test is preferred
- Check the ACTH level prior to the test!
- After giving the standard-high dose of 250mcg of synthetic ACTH, a cortisol is checked 1 hour later and if <18, confirms the diagnosis of adrenal insufficiency
- If the patient has AI, then look at the ACTH (which will take some time to result anyway)
- If normal (inappropriately so) or low, this is ACTH dependent AI, also known as central AI (in secondary the problem is the pituitary and in tertiary, the problem is in the hypothalamus)
- If high, then this is ACTH-independent AI, also known as primary AI (AKA the problem is with the adrenal gland)
Causes of Primary AI and Secondary AI
- The causes for both are lengthy, but remember the most common etiology for each!
- The most common cause of primary AI in the developed world is autoimmune adrenalitis
- The most common cause of central AI is discontinuation of glucocorticoids
Today, we presented an interesting case of a young man with no past medical history who presented with two weeks of progressive headache and fever, now with nausea, vomiting, and an episode of transient blurred vision. CSF revealed an elevated white blood cell count with lymphocytic predominance, low glucose, and elevated protein. Serum and CSF CrAg subsequently came back positive and fungal blood cultures showed Cryptococcus Neoformans.
Illness script for Crypto Meningitis:
Epi: AIDS patients with CD4<100
Symptoms: Indolent onset 1-2 weeks for fever, malaise, and headache. Can develop meningeal signs, altered level of consciousness, and focal neuro deficits. Disseminated disease can include pulmonary symptoms and skin findings resembling molluscum contagiosum.
Diagnosis: Serum and CSF CrAg with 93-100% sensitivity and 93-98% specificity. Crypto can be isolated on India Ink stain of CSF 60-80% patients.
Treatment: Induction with 2 weeks of IV amphotericin B and PO flucytosine, consolidation for 8 weeks with high dose fluconazole, and maintenance for one year with low-dose fluconazole. Serial LPs for ICP control. Start ART 2-10 weeks after starting antifungal treatment (delayed due to risk of IRIS).
Today we discussed an impressive diagnostic mystery of a young woman with chronic neck pain and paresthesias who was later found to have a diminished ipsilateral pulse and a SBP of > 60 points in the affected arm compared to the contralateral arm!
The case highlighted a few, highly important points – first – that the pulse examination is paramount in the patient with paresthesias of an extremity.
A broad differential for diminished/absent radial pulse includes atherosclerosis (i.e PAD), embolism, vasculitis (i.e GCA and TA, less commonly Beurger Disease), anatomic (dissection, thoracic outlet obstruction, thrombosed aneurysm) and iatrogenic (i.e post ABG, vasopressors). When you notice unequal pulses in a patient with symptoms relating to that extremity, you must treat this as an emergency!
We then reviewed the distinguishing characteristics of GCA and TA
The key takeaway to remember is that TA is a chronic disease, filled with relapses and therefore these patients must be diligent about their immunosuppression, which in some cases may be lifelong at very low doses.
For those of you who are still here, a historical treat is your reward. At the 12th Annual Meeting of the Japan Ophthalmology Society held in 1908 in Fukuoka, the young Dr. Mikito Takayasu presented a curious case of vascular malformations of the eye. Two of his colleagues, Drs. Katsutomo Onishi and Tsurukichi Kagoshima also presented similar findings, but noted absence of pulses as well. The findings are impressive, but even more impressive is a subspecialist examining the entire body in a patient they were concerned about, a truly admirable – but increasingly uncommon – practice!
Today’s case, brought to us by Dr. Tuan Nguyen, was a middle-aged woman who presented with sore throat and globus sensation, which persisted for >6 weeks before she received a tonsilar biopsy that showed Treponema pallidum, consistent with secondary syphilis.
We went over a strategy of evaluation of the adult patient with acute pharyngitis. First, we ruled out any emergency by evaluating for airway compromise (respiratory distress, tripoding, “sniffing,” stridor), signs of epiglottitis or deep neck space infection (muffled/hot potato voice, drooling, bulging of the structures of the pharynx or palate, torticollis, neck pain/stiffness/swelling, trismus), or sepsis. We then evaluated for the likelihood of Group A strep infection with the Centor criteria. If left untreated, group A strep pharyngitis can lead to rheumatic fever, rheumatic heart disease, glomerulonephritis, and abscess. Then, we took a detailed sexual history to risk stratify the patient for acute HIV, gonococcal pharyngitis, and syphillis.