Epidural Hematoma (quick review)

2 Dec

submitted by Christina Brown, M.D.

37860tn

Definition – Inward bending of cavarum causes bleeding when dura separates from skull:

  • Middle meningeal artery is involved in bleed >50% of time.
  • Meningeal vein is involved in 1/3.

 

Associations 

  • Mortality is 12% and is related to preoperative condition.  
  • Skull fracture is associated in 75% of cases, less commonly in children. 

 

Pediatric Considerations

  • Head injury is the most common cause of death and acquired disability in childhood.  
  • Bleeding is more likely to be venous.
  • Good outcome in 95% of children <5 yr

 

History

  • LOC: 85% will have at some point in course:
  • Only 11–30% will have a lucid interval.

 

MORE Pediatric Considerations

  • Many times the only clinical sign is drop in hematocrit (Hct) of 40% in infants.
  • Bulging fontanel with vomiting, seizures, or lethargy also suggest EDH in infants.
  • Less than 50% of children have LOC at time of injury.
  • Posterior fossa lesions are seen more commonly in children.

 

Physical Exam

  • Pupillary dilation:  Usually on same side as lesion (90%)
  • Hemiparesis >1/3:  Usually on opposite side from lesion (80%)

 

Imaging (CT Head)

  • Lenticular, biconvex hematoma with smooth borders may be seen.
  • Mixed density lesion may indicate active bleeding.
  • Most commonly seen in temporal parietal region

 

 

 

Initial Stabilization/Therapy

  • Head-injured patients have 25% improved mortality when triaged to regional trauma centers
  • Prevent hypoxia and hypotension:
    • Rapid-sequence intubation for signs of deterioration or increased intracranial pressure (ICP)
  • Perform rapid neurologic assessment

 

ED Management

Early surgical intervention (<4 hr) in comatose patients with EDH.  Nonsurgical intervention in asymptomatic patients is associated with high rate of deterioration; >30% require surgical intervention.

Control ICP

  • Prevent pain, posturing, and increased respiratory effort
  • Elevate head of bed 15–20% after adequate fluid resuscitation.
  • Controlled ventilation to PCO2 of 35–40 mm Hg (Avoid hyperventilation unless signs of brain herniation are present).

Continuous end tidal CO2 monitoring

Arterial line placement for close monitoring of MAP, PO2, PCO2

Treat HTN:  Nicardipine, Labetalol

Treat hyperglycemia if present: Associated with increased lactic acidosis and mortality in patients with TBI

Treat and prevent seizures: diazepam, levitiracetam, etc.

and once again, Early (neuro)surgical intervention


 References:

  1. Schaider, J. & Barkin, R. & Hayden, S. & Wolfe, R. & Barkin, A. & Shayne, P. & Rosen, P. (2011). Epidural Hematoma, Rosen & Barkin’s 5-Minute Emergency Medicine Consult.
  2. Bullock M R et al.: Surgical management of traumatic brain injury. Neurosurgery.2006; 58(3 Suppl):S16–S24.
  3. Marion D M.: Epidural hematoma.  In: Bradley W G: ed. Neurology in Clinical Practice,5th ed.Elsevier;2008: 54 A,B:1083–1114.
  4. Vincent J L and Berre J.: Primer on medical management of severe brain injury. Crit Care Med.2005; 33(6):1392–1399.
  5. Huh J W and Raghupathi R.: New concepts of treatment in pediatric traumatic brain injury. Anesth Clin.2009: 27(2):213–240.
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Pyelonephritis (quick hits)

8 Nov

submitted by Christina Brown, M.D.

Definition – Ascension of bacteria from lower urinary tract infection (UTI) into the upper pyelourinary tract. Primarily a clinical diagnosis.

 
Epidemiology of Male/female ratio:
• 1:10 in 1st years of life
• 1:5 in children
• 1:50 in reproductive years
• 1:1 in fifth decade and later

 
Bacteriology: Escherichia coli 80–95% predominates.

 
Risk Factors – Recent instrumentation, urinary obstruction, urinary retention, recent pyelonephritis (within 1 yr), anatomic variation, neurogenic bladder, DM, immunosuppression, pregnancy.

 
Signs & Symptoms
– Dysuria, urgency, frequency
– Back, flank, or abdominal pain
– Fever, chills, N/V, Malaise
– CVA Tenderness or suprapubic TTP

 

Pediatric Considerations
– Renal scarring: More common sequelae in young children than in adults.
– Group B streptococci

Geriatrics – AMS, nausea/vomiting, diarrhea, fever may predominate.

Urine Culture: >100,000 colony-forming units (CFU)/mL is (+).

CT Imaging:

Consistent or concerning findings:
• Stranding or inflammation and edema of parenchyma
• Perinephric fluid
• Calculi, obstruction
• Renal/perinephric abscess
• Intraparenchymal gas formation (consistent with emphysematous pyelonephritis)

ED Treatment – 14 days duration
– Oral Antibiotics – Ciprofloxacin, Cefdinir
– PEDS – Amoxicillin, Keflex
– IV Antibiotics – Ceftriaxone, Ciprofloxacin
– PEDS 0-3 months – Amp + Gent, Cefotaxime. 3+ months – Ceftriaxone may be used in place of Cefotaxime.

Additional Pediatric Considerations
All children with 1st episode of pyelonephritis should have urinary tract imaging performed later with pediatrician.

Renal US:
• Within 48 hr if no clinical improvement
• Within 3–6 wk if clinical improvement
Girls 4–10 yr old: Voiding cystogram for UVR w/ pediatrician
Boys 4–10 yr old: Voiding cystourethrogram after urine is sterile and bladder spasm has subsided

Disposition

– Admit septic, unable to tolerate PO intake, immunocompromised.

– If clinically stable, discharge home w/ pediatrician f/u within next 48 hrs with appropriate antibiotic regimen.

 

References:

1. Bitner M, Schaider, J., lfe, R. & Barkin, A. & Shayne, P. & Rosen, P. (2011). Pyelonephritis. Rosen & Barkin’s Five Minute Emergency Medicine consult.

2. Piccoli B G, Cresto E, and Ragni F et al.: The clinical spectrum of acute uncomplicated pyelonephritis from an emergency medicine perspective. Int J Antimicrob Agents. 2008; 31(suppl S):S46-S53.

3.  Stunnell H, Buckley O, and Feeney J et al.: Imaging of acute pyelonephritis in the adult. Eur Radiol. 2007; 17:1820-1828.

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Pancreatitis (quick hits)

1 Nov

submitted by Christina Brown, M.D. 

Definition – Inflammation of pancreas due to activation, interstitial liberation, and digestion of gland by its own enzymes. Gallstones and alcohol abuse most common causes.

Acute – Exocrine and endocrine function of gland impaired for weeks-months. Function will return to b/l.

Chronic – Dysfunction progressive and irreversible.

Signs and Symptoms

  • Abdominal pain: 95–100%
  • Epigastric tenderness: 95–100%
  • Nausea and vomiting: 70–90%
  • Low-grade fever: 70–85%
  • Hypotension: 20–40%
  • Jaundice: 30%
  • Grey Turner/Cullen sign: <5%

 

Ranson Criteria – Indicators of morbidity and mortality:

o 0–2 criteria: 2% mortality
o 3 or 4 criteria: 15% mortality
o 5 or 6 criteria: 40% mortality
o 7 or 8 criteria: 100% mortality

Criteria on admission:

• Age >55 yr
• WBC count >16,000 mm3
• Blood glucose >200 mg/dL
• Serum lactate dehydrogenase >350 IU/L
• AST >250 IU/L

 
Diagnostic Evaluation/Labwork

Lipase: Rises within 4–8 hr of pain onset. More reliable indicator of pancreatitis than amylase

Amylase: Levels >3 times limit of normal suggest pancreatitis.

Calcium: Hypocalcemia indicates significant pancreatic injury.

Imaging
Abdominal Series – Most common finding is isolated dilated bowel loop (sentinel loop) near pancreas.

CXR: Pleural effusion

RUQ U/S: Useful if gallstone pancreatitis is suspected.

Abdominal CT indications:

• High-risk pancreatitis (>3 Ranson criteria)
• Hemorrhagic pancreatitis
• Suspicion for pseudocyst
• Diagnosis in doubt

Endoscopic retrograde cholangiopancreatography (ERCP) – Indicated for severe pancreatitis with cholangitis or biliary obstruction

 

 
ED Treatment
Fluid resuscitation

Correct electrolyte abnormalities

• Hypocalcemia (calcium gluconate)
• Hypokalemia occurs with extensive fluid losses.
• Hypomagnesemia occurs with underlying alcohol abuse.

Analgesia, Antiemetics

Antibiotics: Indicated if pancreatic necrosis >30% on abdominal CT

 

DISPOSITION:
Admission Criteria
• Acute pancreatitis with significant pain, nausea, vomiting
• ICU admission for hemorrhagic/necrotizing pancreatitis

Discharge Criteria
• Mild acute pancreatitis without evidence of biliary tract disease and able to tolerate oral fluids
• Chronic pancreatitis with minimal abdominal pain and able to tolerate oral fluids. All discharged mild pancreatitis should have scheduled follow-up within 24–28 hr.

 

References:
Lewis, T. Schaider, J. & Barkin, R. & Hayden, S. & Wolfe, R. & Barkin, A. & Shayne, P. & Rosen, P. (2011). Pancreatitis. Rosen & Barkin’s 5 minute Emergency Medicine Consult.

Frossard D, Steer M L, and Pastor C M.: Acute pancreatitis. Lancet. 2008; 371:143–152

Heinrich S, Schäfer M, and Rousson V et al.: Evidence-based treatment of acute pancreatitis: A look at established paradigm. Ann Surg. 2006; 243(2):154–168.
Hayerle J, Simon P, and Lerch M M.: Medical treatment of acute pancreatitis. Gastroenterol Clin North Am. 2004; 855–869

 CVA (quick ED algorithm)

28 Oct

submitted by Amit Kumar, M.D.

Cerebrovascular Accident: First thoughts…

1) Monitor/stabilize ABCs > POCT glucose > rush to neuroimaging

2) CT/MRI DWI: to differentiate ischemic vs hemorrhagic

3a) If ischemic and within 4.5 hours of last normal: tPA (alteplase)

–0.9mg/kg: Load with 10% (0.09mg/kg) as an IV bolus over 1 minute, followed by 90% (0.81 mg/kg) gtt over 1h

3b) If ischemic and within 6 hours of last normal: endovascular thrombectomy

 

*tPA highly suggested for NIHSS 4-22. Check contraindications.

*Use modified NIHSS (on MDCalc, greater inter-rater reliability, easier)

 

Simultaneous thoughts:

-Have broad differential:

  • hypoglycemia
  • seizure/post-seizure todd’s paralysis
  • infection-induced
  • tox-induced
  • cardiogenic (ex: ACS/STEMI)

 

-No need to micromanage glucose. Reduce if >180 mg/dL, obviously treat if <50 mg/dL

-BP management:

  • If giving tPA (maintain BP <180/110), if not giving tPA (don’t treat unless >220/120).
  • Use titratable IV anti-HTN drugs like labetalol pushes or nicardipine gtt

-Other things that need to happen inpatient (not ED!): HLD panel, HbA1c, carotid dopplers, ECHO, counseling to quit smoking, starting anti-platelet agents (if given tPA, 24 hours after)

 

References:

-Ischemic CVA: https://www.uptodate.com/contents/initial-assessment-and-management-of-acute-stroke?source=search_result&search=CVA&selectedTitle=1~150

-Modified NIHSS: http://www.mdcalc.com/modified-nih-stroke-scale-score-mnihss/

-tPA contraindications: https://www.uptodate.com/contents/image?imageKey=NEURO%2F71462&topicKey=NEURO%2F16134&rank=1~150&source=see_link&search=tpa%20contraindications

Necrotizing Fasciitis (quick-hits)

10 Oct

submitted by Amit Kumar, M.D.

Diagnosis:

1) Physical exam

-pain out of proportion of external appearance of skin, crepitus, dish-water foul-smelling fluid; rapidly progressive

 

2) Criteria: LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score

  • CRP >/= 150: 4 points
  • WBC 15-25: 1 point; >25: 2 points
  • Hgb 11-13.5: 1 point; <11: 2 points
  • Na <135: 2 points
  • Creatinine >1.6: 2 points
  • Glucose >180: 1 point

General rule of thumb:

-Score <6: Low risk but not “no risk” (use history, PE, and clinical gestalt)

-Score >6: +NF (PPV of 92% and NPV of 96%)

 

3) Imaging

-CT without contrast (best at assessing for gas within fascial planes)

necfasc_abd-wall

 

Treatment:

  1. Early and aggressive surgical exploration and debridement
    • debridement of all necrotic tissue until healthy, viable tissue is reached
    • reevaluate in OR ~24 hours later, redebride as needed
  2. Broad-spectrum empiric antibiotics
    • Acceptable regimen: carbapenem/b-lactam and b-lactamase + clindamycin + anti-MRSA (example: meropenem/zosyn or unasyn + clindamycin + vanc/linezolid/daptomycin)
  3. Hemodynamic support
  4. +/- hyperbaric oxygen, IVIG?

References:
-UpToDate (https://www.uptodate.com/contents/necrotizing-soft-tissue-infections?source=search_result&search=necrotizing%20fasciitis&selectedTitle=1~101)

-MDCalc (http://www.mdcalc.com/lrinec-score-for-necrotizing-soft-tissue-infection/)

-Picture of CT scan of abdominal wall abscess (http://bariatrictimes.com/necrotizing-fasciitis-of-the-abdominal-wall-after-laparoscopic-roux-en-y-gastric-bypass-by-joanna-r-crossett-md-and-william-v-rice-md/)

Captain Morgan hip reduction

4 Aug

quick review of this technique, which works great, and takes much less effort than standing on the bed breaking a sweat (my personal recent N of 3 in recent months has been a 3 for 3 success rate)

CONCEPT:tumblr_lriey37dpa1qafl51o1_1280

Provider’s leg up on the stretcher, a-la Captain Morgan’s pose.

Patients leg bent over provider’s thigh

Provider pushes up with their foot, pulls down (lever-action) on patient’s lower leg

Pop’s back into place.

VIDEO ASSIST: (start at the 0:45 mark if you’re short on time)

 

ORIGINAL ARTICLE (Hendey & Avila):

12/13 successful reduction; only failure had an intra-articular fragment that needed the OR

 

There you go. Add it to the toolbox.

 

References: video, picture, article

 

Calcaneal Fracture

15 Jul

submitted by Christina Brown, M.D.

 

Definition – Fracture of the calcaneus secondary to fall from significant height. calcaneal_fracture Attributed to shear stress adjoined with compressive forces combined with a rotary direction.  The calcaneus, also known as the heel bone, is the largest of the tarsal bones and articulates with the cuboid bone anteriorly and the talus bone superiorly.

 

Signs and Symptoms

Most common symptoms = pain upon plantar flexion and palpation of heel.  

Other symptoms include: Inability to bear weight, limited mobility. 

“Mondor sign” = Hematoma extending to sole of foot; pathognomonic for calcaneal fracture [3].   

Associations – Vertebral compression fractures occur in approximately 10% of these patients [1].  A trauma-focused clinical approach should be implemented to evaluate for tibial, knee, femur, hip tenderness.

 

Diagnostic Imaging:

Xray’s – Recommended views = Axial, AP, Oblique [1].

CT – Best for visualization of subtalar joint

 

Intraarticular vs Extra articular:

Intraarticular fractures = more common and tends to involve the posterior talar articular facet of the calcaneus. 

  1. Type I – Non-displaced fractures (displacement < 2 mm).
  2. Type II – Single intraarticular fracture that divides the calcaneus into 2 pieces.
  3. Type III – Two intraarticular fractures that divide the calcaneus into 3 articular pieces.
  4. Type IV – More than three intraarticular fractures.

 

Treatment:

Non-surgical treatment is indicated for intraarticular fractures and Sanders Type I intraarticular fractures. Recommendations include no weight-bearing for a few weeks followed by range-of-motion exercises and progressive weight bearing for a period of 2–3 months.

Displaced intra-articular fractures require surgical intervention within 3 weeks of fracture, before bone consolidation has occurred. 

 

Complications:   Skin blisters may become infected if medical attention is delayed, which can lead to necrotizing fasciitis or osteomyelitis, causing irreparable muscle/bone damage [4].

 

References:

  1. Stoller, D. W.; Tirman, P. F. J.; Bredella, M. (2004). “Ankle and foot, osseous fractures, calcaneal fractures”. Diagnostic imaging: orthopaedics. Salt Lake City: Amirsys. pp. 70–4.
  2. Calcaneus Fractures at eMedicine
  3. Richman, JD; Barre, PS (1986). “The plantar ecchymosis sign in fractures of the calcaneus”. Clinical Orthopaedics and Related Research (207): 122–5.
  4. Heier, Keith A.; Infante, Anthony F.; Walling, Arthur K.; Sanders, Roy W. (2003). “Open Fractures of the Calcaneus: Soft-Tissue Injury Determines Outcome”. The Journal of Bone and Joint Surgery. American Volume 85–A (12): 2276–82.
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