Grand Rounds Recap 5.31.2017

Clinical Soapbox with Dr. McKean

Case: Male in his 50s who presented with 2 weeks of abdominal pain with an abrupt change this morning, tachycardic, lactate of 6.9 and H/H 3.2, perforated viscous on CT of the abdomen. 

Learning Points: 

  • Increased Respiratory Rate can mean acid is present
  • Concerned about perforated viscous? Put the CT on lung fields to find free air
  • Study what scares you


  • Who gets it?
    • Iatrogenic
      • Endoscopy/Colonoscopy
      • Rigid v Flexible (0.11% v 0.03%)
    • Trauma
      • CT Sensitivity
        • Bowel injury 87%-95%
        • Some studies site as low as 80%
      • Seat Belt Sign
    • Medications
      • Upper GI ulceration (NSAIDS/Corticosteroids)
      • Diverticular perforation
        • Opioids: OR 1.8
        • NSAIDs: OR 4.0 
        • Corticosteroids: OR 7.0
    • Infectious/Inflammatory
      • Appendicitis
      • Diverticulitis
      • Crohn's Disease
    • Ischemic Bowel
      • Vascular/Thromboembolic
    • Neoplasm
      • Direct erosion
      • Obstruction
      • Radiation
      • Gastric Cancer during Chemo (1.7%)
  • Physical Exam
    • What's spilling?
    • Where's it spilling?
    • Can they feel it spilling?
  • Diagnosis
    • Plain film images
      • Only 50-70% sensitivity for free air
    • Special Circumstances: Post-operative
      • Pneumoperitoneum
        • Seen in 44% of patients at 3 days post operative
  • Therapy
    • Antibiotic Therapy
      • GN and Anerobic coverage
        • Zosyn
        • Cipro/Flagyl
    • Antifungal Therapy
      • If the perf is proximal to ligament of Treitz
  • Management
    • Manage the sepsis
    • Surgical Intervention

R2 Case Follow Up: Dr. Murphy

Middle aged female with history of MRDD, epilepsy s/p temporal lobectomy presenting from nursing facility, experiencing seizures, received 4 mg lorazepam en route.  Estimated seizure time of 30 minutes.  Received additional 10 mg IM midazolam by EMS.  Febrile to 102.  Exam shows LUE shaking and left gaze deviation.  

Status Epilepticus

2012 NCS Guidelines define as 5 minutes or more of seizure activity or seizure activity without return to baseline

  • Reported mortality 8-20%
  • <50% of patients with status have diagnosed epilepsy
  • Hypoxia and anoxia as cause of status has large mortality
  • Reversible causes 
    • Hypoglycemia
    • Hyponatremia
      • Treatment goal to increase Na levels by 4-6 mEq/L
  • Eclampsia
    • Delivery for definitive treatment

Stages of status

  • Early: before any treatment provided
    • Treat with benzodiazepines
    • RAMPART Trial: NEJM
      • Compare IM midazolam 10 mg vs 4 mg IV lorazepam in pre-hospital setting
      • IM midazolam found to be non-inferior
  • Established: 1st agent (benzodiazepines) has failed
    • Treat with second line agent
      • Poor evidence, efficacy between agents ranges from 50-70ish%
      • ESETT Trial currently studying fosphenytoin vs valproic acid, vs levetiracetam
  • Refractory: 2nd agent has failed
    • 31-43% of patients enter this stage
    • Mortality in range of 30-40%
    • Poor data about efficacy of treatment, possible trend towards propofol being advantageous over barbiturates
    • Secure the airway at this stage if not already established
  • Super-refractory: 3rd agent has failed, activity passing 24 hours
    • Only 4% of patients
    • Almost no evidence
    • Postulated to be higher incidence of autoimmune
    • May consider plasmapheresis/IVIG
    • Intubation medications in status
      • Sedative: no good literature
        • Consider propofol or ketamine, both with some anti-epileptic function
      • Paralytic
        • Rocuronium, etc has disadvantage of losing neuro exam for longer
        • Succinylcholine, theoretic risk of potassium elevation with sustained seizure


Clinical Pitfalls in Neurology with Dr. Neel

Case 1

Young female with lupus and asthma history presenting to outside hospital with 3 day history of worst headache of life and stiff neck.  Ran out of prednisone one month earlier, no other immunosuppressive therapies.  Recent otitis media treated with amoxicillin.  On exam appears uncomfortable and resists neck movement, neurologic exam is otherwise intact with the exception of unable to perform gait assessment as patient reported pain too severe to walk.  Initial head CT shows right parietal hypo density with subarachnoid blood and 3-4 mm midline shift.

    - Parietal lobe is difficult to localize on exam, be cautious of writing off focal problem in setting of poor participation on exam 

LP shows 901 RBC, 90 WBC (75% neutrophils), only one tube available for studies.  Glucose not terribly deranged in CSF.  MRV shows right proximal internal jugular vein, transverse sinus and sigmoid sinus clotted off.  Antibiotic coverage broadened to include pseudomonas coverage.  Unfortunately patient with persisting and worsening headache, CT showing more midline shift.  Moved to ICU to initiate hypertonic saline therapy.  Worsening images concerning for subacute infarct vs abscess.  Develops rash, fever and ARDS, intubated in ICU.  Repeat imaging appears more infarct than infectious, surgery postponed at that time.  Worsening coagulation profile.

  • What are we missing?
    • Differential involving lupus
      • Vasculitis
      • Continuing infection
      • Demyelinating disease, autoimmune, etc
      • Neoplasm
      • Anti-phospholipid antibody syndrome
        • Can look like hyper coagulable or demyelinating
    • Diagnosis: Catastrophic Antiphospholipid Antibody Syndrome (CAPS)
      • Severe multi-organ dysfunction with rapid, diffuse, small vessel thromboses
      • Malignant HTN, ARDS, DIC, MAHA
      • Triggers include surgery, OCP use
      • Involvement of >3 organs/systems/tissues
      • Subacute presentation
      • Treat with anticoagulation, high dose steroids, plasma exchange

Case 2

Middle aged female presenting with headache, intractable nausea and vomiting and “spells”, headache progressively worsening over the past month.  Associated with photophobia.  Poor oral intake for 2-3 weeks, leg numbness after steroid injection for back pain.  Bilateral ureteral stent placement for persistent UTI in setting of narrowed ureters.  Pain in upper back on exam, tender to palpation in epigastric region, near exam noted for decreased light touch in dorsum of left foot, 0 reflexes in bilateral lower extremities, antalgic gait.  Afebrile.  White count near 16, CRP 19, other labs normal.  T1 post on MRI shows abnormal enhancement of the cerebellum with extending arachnoid inflammation, probable diffuse meningeal involvement.  MRI of spine with no metastasis.  CSF shows 77 WBC in tube 1, 148 in tube 4, macrophage predominant.  Opening pressure 58.  Progressed to right sided numbness, then diplopia, facial droop and dysarthria, then she developed ptosis, spell with arm flexion lasting 2 minutes, respiratory distress.  Intubated and transferred to ICU.  ANA positive, lyme antibody and IgM positive, however, western blot for lyme negative.  

What are we missing?

  • Went back and re-examined the body.  Found supraclavicular lymph node, positive for poorly differentiated metastatic disease.  Final diagnosis of leptomeningeal carcinomatosis.  
  • Leptomeningeal metastases arising from systemic solid tumors
  • 3rd most common CNS metastasis of systemic cancer and the most morbid
  • Breast, lung, melanoma, acute leukemia are most common causes
  •  Be suspicious of this in setting of cauda equina, communicating hydrocephalus with high ICP, and oculomotor dysfunction

CPC with Drs. McKee and Hill

Elderly female with history of HTN, questionable bipolar disorder, presenting with hallucinations.  Initially taken to PES, sent over to ED for medical clearance.  Found earlier today by daughter naked, talking to the wall, throwing things.  Daughter called police for help.  On exam patient is found to be restless, confused, states “everything hurts”.  Reports she is thirsty.  Visual hallucinations of bugs.  Afebrile, tachycardia to 114, BP 155/114, normal respiratory rate and oxygen saturation.  No other focal findings on exam, psychiatric exam noted for confusion, anxiety, lability, easily distractible.  Normal fingerstick blood sugar, EKG shows sinus tachycardia.   

Diagnostic test: basic metabolic panel for calcium, diagnosis of hypercalcemia

Calcium level of 16.6, ionized calcium level 8.8.

Patient eventually found to be classic primary hyperparathyroidism.

Hypercalcemia found in 1/500 of general population

    - Most in mild range hypercalcemia

    - Hypercalcemic crisis - hemodynamic instability with or without severe CNS depression

Think of everything “slowing down” with hypercalcemia

  • Degree of symptoms correlates with rate of change, not just absolute rise in calcium levels
  • Stones, bones, moans, psychiatric overtones

Cardiac manifestations

  • Calcium gated potassium channels
  • QT shortening
  • Ventricular irritability


  • Aggressive hydration
    • Urine output goal of 200-300 cc/hr
    • Replace K, Mg
  • Hemodialysis

Long term treatment

  • Block access to the calcium
    • calcitonin
    • bisphosphonates
    • corticosteroids

R1 Clinical Diagnostics: LFTs with Dr. Banning

For an in depth look at this talk - please see Dr. Banning's original post at

1.)  Hepatocellular pattern

  • ALT more specific to liver damage
    • Remains elevated for longer and can take weeks to return to baseline
  • AST found in brain, skeletal muscle, kidney, heart in addition to liver
  • Mild elevation (<5x upper limit of normal)
    • Differential
      • Drug induced (Amoxicillin-clavulanate)
      • Alcoholic induced
      • Non alcoholic fatty liver disease
      • Other: many possibilities
        • Primary care literature supports follow up labs in 2 weeks for asymptomatic mild elevation of transaminase levels
  • Moderate elevation (5x-10x)
    • Hepatic congestion
  • Severe elevation (>10x)
    • Viral hepatitis
    • Ischemic injury
    • Acetaminophen toxicity
      • Stage 1: 30 min-24 hours
        • Nausea, vomiting, diarrhea, malaise
      • Stage 2: 24-72 hours
        • Rapid elevation in ALT/AST, hepatic enlargement, RUQ pain
      • Stage 3: 72-96 hours
        • Severe elevation in levels
        • Death most often in this stage
  • Acetaminophen poisoning nomogram
    • Not used after 24 hours post ingestion
    • Levels may be negative by that time
    • Not used in acute on chronic or polyingestion
    • N-acetylcysteine
      • Indications:
        • above nomogram greater than 4 hours
        • level greater than 10 mcg/ml at any time
        • ANY evidence of liver injury
        • Goal to start before onset of liver injury (within 8 hours of ingestion)

2.) Cholestasis pattern    

  • Alkaline phosphatase
    • rises first in cholestasis
    • can be elevated in non-liver pathology (normal GGT level)
    • if elevated alkaline phosphatase and elevated GGT, then must differentiate between 
    • intra-hepatic and extra-hepatic causes
  • Bilirubin
    • Indirect (unconjugated): albumin bound, circulating in blood
    • If indirect level is greater than 90% of total bilirubin, elevation is not related to liver pathology (hemolysis vs gilbert’s disease)
    • Direct (conjugated): water soluble version transported in bile
    • elevated in acute liver failure, liver congestion, etc.

3.) Functional impairment

  • Liver studies in pregnancy
    • Alkaline phosphatase elevates during pregnancy
    • Albumin, GGT decrease
    • INR should not elevate during normal changes of pregnancy