1 and 2 Sep - Stroke potpourri

Two cases this week have been of unusual nerologic deficits in young patients.  One patient presented with an episode of syncope and awakened with a headache and residual hemipareisis.  There was significant sinus bradycardia present and CNS imaging with MRI revealed multifocal lesions consistent with "emboli or vasculitis or small vessell ischemic disease."  The second case was a 27 year old male with R sided weakness and expressive aphasia who was found to have a L MCA distribution stroke.  TTE suggested PFO with shunt, TEE did not reveal any PFO, shunt, or thrombi.  In both patients classic stroke risk factors were not present.

The impact of an atrial septal defect on the risk of recurrent stroke is debated, but the current practice guidelines review from the Neurology journal suggest that an isolated ASD has no impact on recurrent stroke risk.  An ASD associated with an atrial septal aneurysm does appear to increase recurrent stroke risk.  The choice between antiplatelet and anticoagulant therapy is currently weighted towards antiplatelet therapy.  Anticoagulation with warfarin does not clearly improve outcomes and does increase the incidence of minor bleeding.

The evaluation of stroke in young patients (15 - 45 years) encompasses a search for risk factors that are not typical of stroke in older adults.  In a recent review of the topic, atherosclerosis accounted for 21%, cardioembolism in 17%, non-atherosclerotic vascular (migraine, dissection, etc) in 17%, but 36% had undetermined cause. 

Some zebras to consider:

Sneddon syndrome - livedo reticularis associated with ischemic cerebrovascular disease and hypertension.  Antiphospholipid and anticardiolipin antibodies are commonly found.  Usually seen in adult women and the rash follows the stroke.

Moyamoya syndrome (reviewed in May 2009 NEJM) - progressive stenosis of internal carotids in young patients.  Leads to development of distal small vessell collateral ciculation that gives a "puff of smoke" (moyamoya in Japanese) appearance on angiography.  Can lead to ischemic or hemorrhagic stroke.  Cranial XRT, down syndrome, and NF1 predispose to this condition.  Rule of thumb - if a disease is reviewed in NEJM it is fair game for an ABIM examniation question.

Aug 20 - vertebral osteomyelitis and epidural abscess

This mornings case was a 51 year old man presenting with one month of progressive back pain (thoracic) associated with low grade fevers, leukocytosis, and weight loss.  Imaging via CT at an outside facility revealed degenerative changes, spinal stenosis, and not much else.  He presented here febrile with some lower extremity spasticity but no bowel or bladder dysfunction.  he did have decreased sensation in the lower legs.  There was point tenderness over the mid thoracic spine.

There are multiple red-flag symptoms in this back pain presentation.  This recent evidence based guideline from Annals identifies some common alert signs and presents an algorithm for workup:

In this case the patient was found to have vertebral osteomyelitis an epidural abscess due to methicillin susceptible Staphylococcus aureus and was taken for surgical decompression.  He is in the early stages of an 8 week course of IV antibiotics. 

Some key points:

Medical therapy with IV antibiotics alone is appropriate therapy for select patients with epidural abscess according to this Arch Int Med study.  This is a bit of a change from previous dogma.

There are no practice guidelies dictating duration of therapy, with differing opinions regarding duration of therapy.  I generally choose 8 weeks, but this NEJM review from March 2010 suggests a duration of 6 weeks for most patients.

Regarding the efficacy of vancomycin compared to nafcillin for MSSA - see these articles:

AAC Jan 2008 - mortality with vanco 37% compared with 18% treated with beta-lactams.
Medicine Sep 2003 - study of MSSA bacteremia without endocarditis - failure rate with vanco near 20% compared with no failures in the nafcillin group.

The bottom line is beta lactams are clearly superior to vancomycin in S aureus infections, and in the case of serious or life threatening S aureus infections I feel it is worthwhile to desensitize to beta lactams in order to use these agents if at all possible.

Aug 19 Syncope and Pulmonary Hypertension

This case was an elderly female with previously repaired aortic stenosis (mechanical AVR 15 years prior) who presented with recurrent syncope over the past 1 - 2 years.  The syncope occured with exertion and was increasing in frequency.  She carried a diagnosis of hypoxemic "COPD" but no PFT records were available.  PaO2 was low, and there was no evidence of CO2 retention.  She was suspected of having pulmonary hypertension by ECHO but had refused R heart catheterization to confirm. 

Will not go into discussion of syncope workup here - see this post from July 7.

Effort syncope has been described as a common symptom in primary pulmonary hypertension for quite some time.  An early effiort to identify the mechanism found progressive decreases in blood pressure ultimately resulting in acute R heart failure accounted for the syncopal attacks.  Tachy or brady arrhtyhmias occured but did not seem to be responsible for the acute drop in BP.

A nice review of primary pulmonary hypertension from AAFP is here.

Aug 18 - Lupus Flare

Today's case was a patient with a known prior history of SLE that presented with multiple complications - including fevers, arthralgias and myalgias, and a rash on her face and abdomen.  Workup revealed evidence of multisystem disease, with elevated cardiac enzymes, hematuria, anemia, and thrombocytopenia.  Complicating her picture was a recent hospital stay where she rec'd heparin, and anti-heparin antibodies were positive. 

Peripheral blood smear revealed schistocytes:

Click this link for a nice review of mircoangiopathyc hemolytic anemia from the American Society of Hematology Image Bank

The working differential was HIT/HAT vs TTP vs other thrombotic microangiopathy.  TTP incidence is elevated in patients with SLE, and autoantibodies to ADAMTS-13 seem to play a role in pathogenesis.

Here is a link to another review of SLE pathogenesis in general from a recent NEJM article.

11 August - cholangitis

Running behind on blog updates due to a recent plague visitation at the Rasnake house. 

Two cases recently presented of patients with biliary tract complications.  One was a patient with fever, jaundice, and leukocytosis with a history of previously instrumented biliary tract due to carcinoma - diagnosis was cholangitis. 

Charcot's triad: rever, RUQ pain, and jaundice
Reynold's pentad: above three plus mental status change and hypotension.

Broad spectrum antibiotics to cover gram negative rods and anaerobes are important, but the key to management is decompression of the biliary tree via ERCP or other invasive methods.

The other case was a patient with a progressive mass in the vicinity of the pancreas but separate from pancreatic tissue that had been slowly enlarging over many months.  Most likely diagnosis in this case is lymphoma pending tissue biopsy.

Friday I was out due to monthly residency review meeting - regular updates will resume this week.

23 Jul - Pleural Effusion

This AMs case was a patient who presented with dyspnea and R chest pain 6 weeks following an episode of pneumonia.  CXR revealed a large R sided pleural effusion.

Thoracentesis was performed with findings of cloudy fluid with a protein ratio <0.5 but an LDH ration >0.6, consistent with an exudate.  No organisms were seen on gram stain and the glucose and cell counts were unremarkable.

Since we are not doing thoracentesis yet in the sim lab - you all should at least review the video here at the NEJM website before peforming this procedure.  Common ommisions that I have witnessed include not having the patient fully exhale and hold their breath when removing the catheter from the chest at the completion of the procedure.

To interpred the results of the pleural fluid analysis, consult these articles here and here by the guru of pleural fluid analysis Dr Light.  His criteria show up frequently on exams and challenge bowls:

pleural fluid / serum protein ratio >0.5
pleural fluid / serum LDH ratio >0.6
pleural fluid LDH > 2/3 the upper limit of serum normal value

Any one is sufficient to diagnose an exudative effusion, but the specificity is only 82 - 83%

Light's criteria are the most sensitive (98%), but a serum albumin - pleural albumin of <= 1.2 or a pleural fluid cholesterol >= 60 are both more specific at 92%

22 Jul - Pulmonary Embolism

This AMs case was a patient admitted with subacute onset of dyspnea.  Initial evaluation revealed an elevated D-dimer, swollen LLE and normal CXR.  CT PE study revealed extensive bilateral PEs with proximal involvemetn and R heart strain.  He had made several recent long car trips but had no other known predisposition to thromboembolism. 

For a recent summary of acute PE management see this NEJM review from this past week's issue.

Regarding selection of PE patients for outpatient treatment or early discharge - know that the data to support this practice is of poor quality and that patients with hypoxemia, RV dysfunction, large proximal PEs, and obesity (>110 kg) were excluded from the studies of outpatient treatment.  These individuals should be managed as inpatients until oral anticouagulants are at therapeutic levels and clinical stability is achieved.  This recent review should be noted before you consider early discharge of a PE patient.