Tag Archives: brown

Epidural Hematoma (quick review)

2 Dec

submitted by Christina Brown, M.D.


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.



  • 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



  • 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


  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.
  6. picture




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.

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


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.


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


9 May

submitted by Christina Brown, M.D.

Definition – Air in the cranial vault.  

Mechanically speaking, intracranial air becomes trapped and expands due to a ball valve effect resulting in mass effect, can result in headache and signs and symptoms of increased ICP [5].  

Usually associated with neurosurgery, barotrauma, basilar skull fractures, sinus fractures, nasopharyngeal tumor invasion and meningitis [1, 2].


  • Headache and altered consciousness are the most common symptoms [3].
  • Tension pneumocephalus = neurosurgical emergency


  • X-rays can diagnose pneumocephalus, but CT scan is the modality of choice.
  • Classical CT sign of tension pneumocephalus = “Mount Fuji sign”: the massive accumulation of air that separates and compresses both frontal lobes and mimics the large volcano in Japan.  




  • Neurosurgery C/S. In the vast majority, post-operative pneumocephalus is an expected finding in essentially all post-craniotomy patients.  Most cases of pneumocephalus resolve spontaneously, and conservative management should be provided.  
  • Non-operative management involves oxygen therapy, keeping the head of the bed elevated, prophylactic antimicrobial therapy (especially in post-traumatic cases), analgesia, frequent neurologic checks and repeated CT scans. 


Operative – In cases of tension pneumocephalus, a burr hole may need to be performed to relieve pressure. 



  1. Yildiz A, Duce MN, Ozer C, et al. Disseminated pneumocephalus secondary to an unusual facial trauma. Eur J Radiol. 2002;42:65–68. doi: 10.1016/S0720-048X(01)00383-7. 
  2. Jenson MB, Adams HP. Pneumocephalus after air travel. Neurology. 2004;63:400–401.
  3. Kapoor T, Shetty P. J Emerg Med. 2008;35:453–454. doi: 10.1016/j.jemermed.2007.03.046. 
  4. Satapathy GC, Dash HH. Tension pneumocephalus after neurosurgery in the supine position. Br J Anaesth. 2000;84:115–117. 
  5. Satapathy GC, Dash HH. Tension pneumocephalus after neurosurgery in the supine position. Br J Anaesth. 2000;84 (1): 115-7. Br J Anaesth (abstract)
  6. pictures


Septic Arthritis (quick review)

24 Nov

Risk Factors:

  • Age >80 years
  • Diabetes mellitus
  • Presence of prosthetic joint
  • Skin infection
  • Rheumatoid arthritis
  • Recent joint surgery
  • Intravenous drug abuse, alcoholism
  • Corticosteroid injection


Bacteremia is more likely to localize in a joint with preexisting arthritis, particularly if associated with synovitis.  Patients with RA may have additional predisposing factors, such as prior intraarticular steroid injections, maintenance immunosuppressive medications, and anti-tumor necrosis factor (TNF) therapy [1]. 


Mechanism:  Hematogenous spread to the joint.   Bacterial arthritis can also arise as a result of a bite or other trauma, direct inoculation of bacteria during joint surgery. 

Because synovial tissue has no limiting basement plate, bacterial organisms can quickly gain access to the synovial fluid, creating acute-onset joint inflammation with purulence. Following onset of infection, there is marked hyperplasia of the lining cells in the synovial membrane within seven days (1).


Differential Diagnosis

Reiter’s syndrome, pseudogout, GC arthritis, Lyme disease, RA, osteoarthritis, reactive arthritis


Clinical Manifestations:

A majority of patients with bacterial arthritis are febrile.  Older adult patients with septic arthritis are less likely to present with fever.  


Joint Aspiration:   Since this condition represents a closed abscess collection, the joint space should be drained. After initiation of treatment, serial synovial fluid analyses should reveal decrease inflammatory burden.


Synovial Fluid Profile

Greater > 2000 leukocytes/ml (5):

  • Traumatic Arthritis – < 5,000  (w/ RBCs) (5)
  • Reactive Arthritis – Recent genitourinary or gastrointestinal signs or symptoms, conjunctivitis, or skin or mucus membrane lesions (1).
  • Rheumatoid Arthritis – 10,000- 15,000 and 50 % polymorphs. Sterile incr protein, & decreased viscosity & decreased complement (5).
  • Toxic Synovitis – 15,000 and less than < 25 % polymorphs (5)

Greater > 50,000 leukocytes/ml (5):

  • Gout/Psuedogout – Synovial fluid analysis to r/in crystals (5).
  • Septic Arthritis – 80,000-200,000 and > 75% polymorphs (5).


ManagementOrthopaedics C/S and antimicrobial therapy

Antibiotic Therapy based on Synovial Fluid Analysis

If (+) GPC, treat w/ Vancomycin 30mg/kg q daily.

If (+) GNR, treat w/ Ceftriaxone 2g IV q daily. Duration of therapy:  Recommend IV x 14 days and transition to PO.

Complications – Cartilage degradation and inhibition of cartilage synthesis. Pressure necrosis from large synovial effusions may result in further cartilage and bone loss (1).


PrognosisInflammation and joint destruction may continue even in the setting of a sterile joint, despite effective antimicrobial therapy [1].


Submitted by Christina Brown, M.D.



  1. http://www.uptodate.com/contents/septic-arthritis-inadults?source=search_result&search=septic+joint&selectedTitle=1~150
  2. Mor A, Mitnick HJ, Greene JB, et al. Relapsing oligoarticular septic arthritis during etanercept treatment of rheumatoid arthritis. J Clin Rheumatol 2006; 12:87.
  1. Margaretten ME, Kohlwes J, Moore D, Bent S. Does this adult patient have septic arthritis? JAMA 2007; 297:1478.
  2. Goldenberg DL. Septic arthritis. Lancet 1998; 351:197.
  1. http://www.wheelessonline.com/ortho/septic_arthritis
  2. picture 1, picture 2

Resuscitative Thoracotomy

17 Sep

A thoracotomy can be a life-saving procedure in a select group of patients.  This specific subset of patients is stillcontroversial. 

Resuscitative thoracotomy may be justified in trauma patients with shock.  The beneficial aspects of the procedure include:

  • decompressing cardiac tamponade
  • cross-clamping the aorta
  • controlling exsanguinating cardiac or large vascular injuries. 

External chest compressions can provide a maximum of 30% of cardiac output and is dependent on venous return to the heart (1).  Chest compressions in the trauma patient are ineffective, may increase cardiac trauma by causing blunt myocardial injury and obstruct access for performing definitive manoeuvers (1).

Penetrating Thoracic Injury — Resuscitative thoracotomy may be justified in patients with:

  1. Hemodynamically unstable on arrival AND after appropriate fluid resuscitation.
  2. Pulseless patients, receiving CPR for less than 15 minutes, and if appropriate resources (eg, appropriately-trained surgeon, operating room) are available [4].

Blunt Thoracic injury — controversial.  According to the American College of Surgeons the sector of patients who may benefit include:

  1. Cardiac arrest in a trauma patient occurring prior to ED arrival, during resuscitation or observation
  2. Profound hypotension (BP<70mmHg) due to truncal wound in an unconscious patient or unavailable operating room.

Contraindications — Resuscitative thoracotomy is likely to be futile if:

  • No signs of life at the scene of injury
  • Asystole is presenting rhythm and no pericardial tamponade on U/S.
  • Prolonged pulselessness (>15 minutes)
  • The patient requires >10 minutes of prehospital CPR
  • Multiple, massive non-survivable injuries.
  • Severe head injury (1)

PREPARATION — One member of the trauma team should be designated to lead the ongoing resuscitation effort while an experienced member of the trauma team is performing the thoracotomy.

General Approach

A left sided approach is used in all patients in traumatic arrest and with injuries to the left chest. Patients who are not arrested but with profound hypotension and right sided injuries have their right chest opened first (4)

  • An anterior lateral incision is made, the chest is entered, and a retractor is placed. Left or right incision based on location of thoracic injury.
  • If tamponade is present, perform pericardiotomy – The pericardial sac is opened and temporizing measures are used to control any cardiac injuries.
  • The aorta is cross-clamped to allow filling of the heart and facilitate ongoing fluid resuscitation.
  • Open cardiac massage using a two hand approach (operator’s thumb can perforate right ventricle) is initiated once the heart has filled sufficiently.

Outcomes — Clinical data evaluating the outcomes of resuscitative thoracotomies are derived primarily from retrospective cases (3-5). Much heterogeneity in the populations and outcomes were present.

COST — Resuscitative thoracotomy is expensive.  Costs associated with other aspects of resuscitative thoracotomy include expenditures related to community EMS, hospital resources including supplies, personnel and transfusion services, and consequences of blood-borne pathogen exposures. Furthermore, the patient neurological outcome plays a critical role in the long-term outcome of patient population.

Submitted by Christina Brown.


  1. http://www.trauma.org/index.php/main/article/361/
  2. http://www.uptodate.com/contents/resuscitative-thoracotomy-technique?source=search_result&search=thoracotomy+adult&selectedTitle=1%7E150#H536270528
  3. Seamon MJ, Shiroff AM, Franco M, et al. Emergency department thoracotomy for penetrating injuries of the heart and great vessels: an appraisal of 283 consecutive cases from two urban trauma centers. J Trauma 2009; 67:1250.
  4. Karmy-Jones R, Namias N, Coimbra R, et al. Western Trauma Association critical decisions in trauma: penetrating chest trauma. J Trauma Acute Care Surg 2014; 77:994.
  5. Slessor D, Hunter S. To be blunt: are we wasting our time? Emergency department thoracotomy following blunt trauma: a systematic review and meta-analysis. Ann Emerg Med 2015; 65:297.
  6. Powell DW, Moore EE, Cothren CC, et al. Is emergency department resuscitative thoracotomy futile care for the critically injured patient requiring prehospital cardiopulmonary resuscitation? J Am Coll Surg 2004; 199:211.
  7. Photo credit via < http://www.trauma.org/index.php/main/article/361/

SVC Syndrome

27 Aug


Your next patient is a 70 yo M with neck swelling and syncopal episode, who said he “felt like couldn’t breathe” when bending forward, then passed out. 

Vital Signs – WNL

Physical exam – Awake, ambulating male with chest wall venous distention, b/l neck swelling, facial plethora when leaning forward and trace peripheral, LE edema. 



Superficial venous distention in superior vena cava syndrome  —>



Imaging – In ED, CT chest and neck (w/ contrast) to evaluate for obstructing mass (e.g. something compressing the SVC)


Etiology – In the preantibiotic era, syphilitic thoracic aortic aneurysms, were frequent causes of the SVC syndrome.  More recently, intrathoracic malignancy is responsible for 60 to 85 % of cases of SVC syndrome.  Non-small cell lung cancer (NSCLC) is the most common, accounting for 50 %  of all cases.

Clinical Manifestations – Interstitial edema of the head and neck is visually striking, but generally of little clinical consequence.  However, edema may narrow the lumen of the nasal passages and larynx –> dyspnea, stridor, cough, hoarseness, and dysphagia.  Cerebral edema can also occur (not awesome).

Cardiac output may be diminished transiently by acute SVC obstruction, but, within a few hours, blood return is reestablished by increased venous pressure and collaterals. Hemodynamic compromise, if present, more often results from mass effect on the heart than from SVC compression.


Submitted by Christina Brown.


References: Up to Date: malignancy related SVC syndromeWilson LD, Detterbeck FC, Yahalom J. Clinical practice. Superior vena cava syndrome with malignant causes. N Engl J Med 2007; 356:1862.SCHECHTER MM. The superior vena cava syndrome. Am J Med Sci 1954; 227:46.Yellin A, Rosen A, Reichert N, Lieberman Y. Superior vena cava syndrome. The myth–the facts. Am Rev Respir Dis 1990; 141:1114.Rice TW, Rodriguez RM, Light RW. The superior vena cava syndrome: clinical characteristics and evolving etiology. Medicine (Baltimore) 2006; 85:37.Chee CE, Bjarnason H, Prasad A. Superior vena cava syndrome: an increasingly frequent complication of cardiac procedures. Nat Clin Pract Cardiovasc Med 2007; 4:226.picture


14 Jul

manifests as:

  • ischemic rest pain
  • ischemic ulcers
  • gangrene



  • Embolus from a proximal source lodging into a more distal vessel
  • dissection of an artery or direct trauma to an artery



  • atrial fibrillation,
  • Recent myocardial infarction
  • Aortic atherosclerosis,
  • aneurysmal disease (eg, aortic aneurysm, popliteal aneurysm)
  • Prior lower extremity revascularization (angioplasty/stent, bypass graft),
  • Risk factors for aortic dissection (HTN, etc)
  • Arterial trauma
  • Deep vein thrombosis (paradoxical embolism)
  • left ventricular dysfunction
  • debris from prosthetic valves and infected cardiac valves (septic emboli)


Arterial Trauma — Acute arterial occlusion following interventional procedures has become a more frequent cause — the incidence of arterial complications following interventional cardiac catheterization is ~1.5 to 9 percent 


6 P’s

  • paresthesia,
  • pain,
  • pallor,
  • pulselessness,
  • poikilothermia,
  • paralysis


Variations Blue toe syndrome — sudden appearance of a cool, painful, cyanotic toe(s) or forefoot in the often perplexing presence of strong pedal pulses and a warm foot.  The blue toe syndrome is usually due to embolic occlusion of digital arteries with atherothrombotic material from proximal arterial sources.


First LineComputed tomographic angiography with runoff, noninvasive duplex ultrasonography, or magnetic resonance angiography



intravenous heparin bolus followed by a continuous heparin infusion 

Preoperative eval, including blood tests (PT/PTT, CBC) and electrocardiography (ECG)

Surgical thromboembolectomy and bypass grafting – Were the mainstays of therapy for many years. Subsequently, thrombolytic therapy and percutaneous transluminal angioplasty (PTA) have become treatment options for selected patients. 

Consult Vascular Surgery.

Submitted by Christina Brown.


References: uptodate.com, Norgren L, Hiatt WR, Dormandy JA, et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). J Vasc Surg 2007; 45 Suppl S:S5Nasser TK, Mohler ER 3rd, Wilensky RL, Hathaway DR. Peripheral vascular complications following coronary interventional procedures. Clin Cardiol 1995; 18:609.Alonso-Coello P, Bellmunt S, McGorrian C, et al. Antithrombotic therapy in peripheral artery disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest 2012; 141:e669S.Yeager RA, Moneta GL, Taylor LM Jr, et al. Surgical management of severe acute lower extremity ischemia. J Vasc Surg 1992; 15:385.; picture