Archive | August, 2012

Pituitary Apoplexy

22 Aug


-Pituitary apoplexy refers to pituitary infarction

-It is a rare condition.  Often occurs spontaneously from hemorrhage or an infarction of a pre-existing pituitary adenoma.  It can also refer to sudden infarction of the pituitary in the absence of a pituitary adenoma.

Pregnancy and trauma have also been associated with the condition.

-Think Pituitary Apoplexy in a patient with sudden severe headache with vision changes and a known history of a stable pituitary adenoma!

-Common precipitating factors include recent major surgery, being on anticoagulation, and hypertension.


-Common symptoms include headache, vomiting, visual field defects, and ocular paresis.

Hyponatremia (caused from SIADH) has also been demonstrated in case reports although it is less common

-Of the ocular palsy findings, 3rd nerve and 6th nerve palsies are most common.


CT scans are generally only useful to find hemorrhage within the adenomas.  This will generally be visible within the first 3 days following hemorrhage, and appear as intrasellar or suprasellar hyperdensity.

MRI is the modality of choice.  Often MRI/MRA are performed to visualize the adjacent carotid arteries to rule out aneurysm as a cause.


-Initial management should include fluids and corticosteroids.  Many patients improve with supportive care alone.

Neurosurgery should be involved early the literature does not appear clear whether supportive measures alone are sufficient or whether patients have an increased benefit from surgical decompression in mild to moderate cases.  In severe cases (vision loss) urgent Neurosurgery involvement and surgical decompression are the standard of care.

-Many patients have significant ocular improvement after either conservative measures or surgery

-The thought is that the optic nerves are particularly able to withstand prolonged ischemia

-Some studies have shown normal vision if the optic nerves are decompressed within a week

Submitted by J. Grover.

References: Agrawal D, Mahapatra AK.  “Pituitary Apoplexy and Inappropriate ADH Secretion.”  Journal of Clinical Neuroscience.  2003 10(2); 26-261. Lubina A, Ochovsky D, Berezin M et al.  “Management of Pituitary Apoplexy:  Clinical experience with 40 Patients.”  Acta Neurochirurgica (wien).  2005 (147): 151-157.  Maccagnan P, Macedo CLD et al.  “Conservative Management of Pituitary Apoplexy:  A Prospective Study.”  J Clin Endocrinol Metab 1995; 80; 2190-2197.  Nawar RN, Abdel Mannan D, et al.  “Pituitary Tumor Apoplexy:  A Review.”  J Intensive Care Med.  2008.  Mar-Apr; 23(2) 75-90. Sibal L, Ball SG, et al. “Pituitary Apoplexy:  A Review of Clinical Presentation, Management and outcome in 45 cases.”  Pituitary.  2004; 7(3): 157-163.; picture

metformin and lactic acidosis

21 Aug


  • decreases insulin resistance,
  • decreases hepatic glucose output,
  • increases glucose uptake peripherally
  • Decreases fasting BG 20-40%.

The major toxic effect of metformin is lactic acidosis.

It causes glucose to be converted to lactate in the small intestines, and decreases gluconeogenesis from lactate– and pyruvate and alanine- increasing LA and substrates that can get converted to LA.

its RARE: Only 5.1 cases per 100,000 patient yrs of lactic acidosis in non-comorbitiy (renal or liver disease) patients.

However in patients that do develop LA, there is a mortality of 45%. These deaths were speculated to be related to comorbid conditions, rather than the levels of metformin in their blood. Most accurate predictor was liver function.

Lactic acidosis likely to occur in patients with renal insufficiency (Cr above 1.4/1.5), liver or ETOH disease, HF, history of prior LA, hypoxic states, hemodynamic instability.


  • consider bicarb if pH < 7.1, otherwise may cause electrolyte abnormalities.
  • Patients with severe renal insufficiency or are simply very sick require emergent HD.

Submitted by J. Rothstein.

References: Risk of fatal and nonfatal lactic acidosis with metformin use in type 2 diabetes mellitus. Salpeter S, Greyber E, Pasternak G, Salpeter E, Cochrane Database Syst Rev. 2006; metformin poisoning; Metformin. AU Bailey CJ, Turner RC SO, N Engl J Med. 1996;334(9):574. picture

Tumor Lysis Syndrome

20 Aug


Oncologic emergency caused by tumor cell lysis (duh)

-Look for tumor lysis syndrome in patients with recent initiation of chemotherapy or radiation, or in cancers with extremely high proliferative rates (Lymphoma and Leukemias). 

-can occur spontaneously as well, most documented in the lymphomas and leukemias, so do not discount the presence of TLS in patients without recent initiation treatment.

-Manifested by both end organ damage and electrolyte abnormalities


Electrolyte Abnormalities: caused by release of intracellular contents

Hyperkalemia caused by the release of intracellular potassium stores can cause arrhythmias

Hyperphosphatemia is often caused.  Phosphorous stores in cancer cells is up to 4 times the normal storage amount found in normal cells- with cell lysis hyperphosphatemia is common.  Calcium can bind to the phosphate forming calcium phosphate precipitation, leading to hypocalcemia.


End Organ Damage

-Release of nucleic acids leads to their catabolism and eventual production of uric acidHyperuricemia can lead to crystal precipitation and deposition in the renal tubules leading to acute renal failure. 

-Precipitation of calcium-phosphate crystals in the renal tubules can also lead to acute renal failure.



Aggressive IV hydration

-Rasburicase is often used to treat hyperuricemia- it is the enzyme urate oxidase which catalyzes the oxidation of uric acid to a safer to excrete renally compound allantoin.

Hyperkalemia can be treated similar to normal managementD50 plus insulin, beta agonists, sodium bicarbonate, and sodium-potassium exchange resins.  HOWEVER calcium administration is generally avoided unless there is evidence of arrhythmia/EKG changes or neurological involvement (seizures), because it can contribute to further production of calcium phosphate crystals and worsen the renal injury.


Submitted by J. Grover.


References: Uptodate.  “Tumor Lysis Syndrome:  Definition, Pathogenesis, Clinical Manifestations, Etiology, and Risk Factors.”  5/30/2012. Uptodate.  “Tumor Lysis Syndrome:  Prevention and Treatment.” Tintinalli 7th Edition.  Chapter 18, pp. 1512-1513.; picture

How to Open an Eye that is Superglued Shut

17 Aug

Cyanoacrylate may contact the eye due to inadvertent administration of superglue instead of eyedrops, rubbing eyes with contaminated hands, or splashing glue into eyes.

Chemical injury is minimal – in fact, ophthalmologists occasionally use cyanoacrylate for intentional tarsorrhaphy and sealing perforated corneal ulcers

Mechanical injury can be significant – from constant movement of eye against fixed foreign body between lids.

Corneal abrasions, eyelash loss, eyelid skin excoriation, or conjunctival inflammation may occur

Irrigate first with room temperature water for 15 minutes

•Rosen’s recommends Ophthalmology consult

•If lids are glued shut, attempt to pull eyelids apart gently

Do not apply substances to dissolve the glue(although gauze soaked in mineral oil and shur-cleans have been reported to work)

•If lids cannot be pulled apart but are aligned normally, and pain is minimal, patient may be discharged. The glue is expected to dissolve over about a week

If the lids are inverted, surgical intervention may be required

Consider discharging with antibiotic ointment for presumed corneal abrasion if full eye exam is not possible.

Submitted by M. Smith.

Reference(s): Lyons C Stevens J, Bloom J. Superglue inadvertently used as eyedrops. BMJ 1990; 300:328; Margo CE, Trobe JD. Tarsorrhaphy from accidental instillation of cyanoacrylate adhesive in the eye. JAMA 1982; 247:660-661; Sharma R, Brunette DD. “Chapter 69: Ophthalmology: Ocular Trauma.” in Rosen’s Emergency Medicine, Concepts and Clinical Practice, 7th ed. Marx et al, eds. 2009, Mosby.;

Poisindex: Cyanoacrylates – Super glue.; picture

colchicine and acute gout

16 Aug


— When seeing a patient during an attack: 1.2mg cochicine then 0.6mg 1 hr later has done well in treating acute gout.

still open whether it compares better than NSAID, glucocorticoid, or IL-1 inhibitors.

— Low dose colcichine was studied in the AGREE trial- showed that lower dose groups ( the 1 day dose or 0.5 TID) had similar effects as the higher dose group with less side effects.

— Subjects in the low-dose treatment group experienced diarrhea (23 percent) or other GI symptoms no more often than placebo-treated subjects (16 percent diarrhea) during the trial, but diarrhea occurred in 77 percent of higher-dose-treated subjects (odds ratio 21.3; CI 8-57). Diarrhea was graded as severe in 19 percent of high-dose treatment subjects versus 0 percent in the low-dose group, and vomiting was seen in 17 percent in the high-dose group but 0 percent in the other groups



–In the end, I think colchicine 1.2mg followed by 0.6mg and follow up with PCP will be my regimen.


Submitted by J. Rothstein.


Reference(s): treatment of acute gout; fda recommendations. picture


Vitreous Detachment or Retinal Detachment?

15 Aug
•Vitreous and retinal detachment have similar symptoms but very different prognosis and treatment. One is an emergency and one seems to be no big deal. How can you comfortably rule out retinal detachment in the ED? Is US helpful?

Both can present with increasing or new flashers and floaters.
  • Sudden onset of one large circular floater in the center of the visual axis indicates a PVD
  • Hundreds of tiny black specks appearing before the eye, followed several hours later by the appearance of cobwebs, is pathognomonic for vitreous hemorrhage
  • New onset floaters with flashers should be considered a retinal tear until proven otherwise
•12% of posterior vitreous detachments have an associated peripheral retinal tear

With retinal detachment, the affected eye may have an IOP 4-5mmg Hg less than the opposite eye

•In an observational study of bedside ultrasound to evaluate for retinal detachment, no cases of retinal detachment were missed by emergency physicians using bedside ultrasound. Sensitivity was 100%, specificity was 83% (5 cases of vitreous hemorrhage were incorrectly diagnosed as retinal detachment).

•Both are indications for ophthalmology consultation

Submitted by M. Smith.

Reference(s): Yoonessi R, Hussain A, Jang TB. Bedside ocular ultrasound for the detection of retinal detachment in the emergency department. Acad Emerg Med. Sep 2010;17(9):913-7; picture

Foreign Body Removal from Ear

14 Aug

•In one retrospective review of 191 aural foreign bodies in children, beads, pebbles, and plastic toys were most common in young children, insects in older children

Irrigation, suction, and instrumentation were all attempted. 30% required surgical removal under anesthesia, and most of these were in children under 8 years old

For irrigation, use a 60cc syringe with a 16g angiocath and body temperature water. Do NOT irrigate disc batteries or objects that may swell (beans, peas)

Objects with sharp edges should be removed with an operating microscope or in the OR

Insects can be killed with microscope immersion oil, mineral oil, or lidocaine, then extracted by irrigation or instrumentation. Microscopic exam is required after removal to r/o retained insect parts

Smooth round objects are very difficult to extract. Try suction

•Complications: EAC lacerations or abrasions, TM perforation, iatrogenic otitis externa

Give antibiotic drops to anyone with inflamed or lacerated EAC after FB removal

•Suggested indications for ENT consultation/referral:
  • –Lack of proper instrumentation
  • –Lack of staff to adequately restrain uncooperative child
  • –Failure to remove foreign body on initial attempt(s)
  • –Existent injury to the external auditory canal or tympanic membrane
  • –Object wedged in the medial external auditory canal or up against tympanic membrane
  • –Glass or other sharp-edged foreign body
  • –Special circumstances such as insects, putty, and disc batteries

Submitted by M. Smith.

Reference(s): Ansley JF, Cunningham MJ. Treatment of aural foreign bodies in children. Pediatrics. 1998 Apr; 101(4 Pt 1):638-41.; picture