Category Archives: DRHEM

04.13.11
by

Intern Report Case Discussion 3.6


Case Presentation by Dr. John Wilburn

Case Presentation (click to see the case)

Answers: 1.b   2.a   3.d   4.a

Discussion:

This patient is suffering from gallstone pancreatitis. Gallstones are the major cause of acute pancreatitis accounting for 40% of cases. Other causes of pancreatitis include alcohol, ERCP induced, medications, metabolic, and idiopathic. Gallstone pancreatitis takes place when a stone impacts and obstructs the ampulla of vater or the pancreatic duct resulting in early activation of exocrine enzymes and auto digestion of the pancreas.  Prognosis is generally good if pancreatitis is mild and appropriately treated. Mortality of mild to moderate gallstone pancreatitis is around 10% which is a decrease in 10-15% over the past 30 years.

Severe pancreatitis is defined by local complications (pseudocyst, hemorrhage, and infection), or signs of organ damage (hypoxia, ARF, DIC, hypocalcemia <7.5). The overall mortality of severe pancreatitis is 30% which has not changed over the past 30 years.

Risk factors for gallstone pancreatitis include: female, advanced age, obesity, multiparous women, high cholesterol, alcoholism, and smoking. 

Most patients have the cardinal symptom of abdominal pain in the epigastric region, but can be in the left or right upper quadrants. Patients usually describe the pain as rapid in onset, constant steady, or boring pain increasing in intensity till it reaches a maximum. When the pain reaches pinnacle with no relief most patients seek medical attention. Patients can present with tachycardia, febrile, and elevation or depression of blood pressure.  This pain can be associated with nausea and emesis and anorexia. Patients can appear jaundiced as obstruction of the ducts causes back up in the biliary system. Most patients on physical exam are tender in the epigastric region and may have a positive Murphy sign.

Pancreatitis should always be in the differential for any patient with upper abdominal pain. The work up for pancreatitis includes cbc, metabolic panel, LFT, and lipase. There is no gold standard diagnosis of pancreatitis most experts agree that lipase is just as sensitive as amylase and has more specificity at 3x normal values. Recently experts in the United Kingdom recommend that lipase should be used for the diagnosis of pancreatitis. Amylase can still be used to diagnose pancreatitis; however it is not as specific at 3x the normal values. ALT above the level of 150IU/L is the most sensitive and specific liver enzyme for gallstone pancreatitis. If pancreatitis is diagnosed ultrasound should be conducted within the first 24 hours to either confirm or rule out gallstones as the cause. CT may also be indicated in severe pancreatitis to rule out peripancreatic complications such as pseudocyst, hemorrhage, and necrosis of pancreas.

Medical management:
Medical management of pancreatitis is usually supportive and tailored to the cause of pancreatitis with emphasis on avoiding complications.  Patients should be admitted to the hospital for intravenous fluids, pain control, antiemetic, and made NPO in the initial phase.  There should be a consult to general surgery for management, ERCP, and cholecystectomy the same hospital admission. Intravenous fluids are the most important intervention in the initial setting, some patients may require up to 6L of fluid as the inflammation leads to sequestration of fluid out of the intravascular space. Give 2-3L bolus of .9ns initially and reassess, if sufficient; place the patient on infusion at 250ml/hr normal saline. Pain control with morphine, no evidence has shown clinical difference or outcome when compared to meperidine.  Nasogastric tube is only indicated in patients with intractable emesis, severe abdominal distention and ileus. Routine use has shown no clinical benefit and has increased the number of days hospitalized. ERCP with sphincterotomy and stone extraction is indicated after the initial pain has subsided and patient clinically improves. This is usually 24-48 hours after admission; early ERCP is only indicated in severe episodes of pancreatitis not responding to conservative management or cholangitis. ERCP may actually induce pancreatitis 5% of the time and is not the definitive treatment for gallstone pancreatitis.  Studies have shown a 30-50% recurrence of gallstone pancreatitis with ERCP alone. Cholecystectomy is the definitive treatment and should be performed on the same hospital admission. Patients with severe pancreatitis require ICU admission.

There are cardiopulmonary, renal, metabolic, infectious, and hematologic complications of pancreatitis. All complications are caused by the inflammatory reaction of pancreatitis. Usually cardiopulmonary collapse due to hypotension or ARDS is the cause of death within the first week. Patients who develop ARDS have a mortality of 50-60% which is the highest of the complications in pancreatitis.

  References
Rosen's Emergency Medicine, seventh edition, 2010, pages 1172-1183, Marx
Tintinalli's Emergency Medicine, sixth edition, 2004, pages 573-577, Tintinalli
Uptodate, Clinical manifestation and diagnosis of acute pancreatitis, 2010, Vege
Pancreatitis, Acute, eMedicine http:emedicine.medscape.com/article/181364
Pancreatitis in Emergency Medicine, eMedicine http://emedicine.medscape.com/article/775867
Dhir, R. et al: Drug-induced pancreatitis: A practical review


04.13.11
by

Intern Report Case Discussion 3.6


Case Presentation by Dr. John Wilburn

Case Presentation (click to see the case)

Answers: 1.b   2.a   3.d   4.a

Discussion:

This patient is suffering from gallstone pancreatitis. Gallstones are the major cause of acute pancreatitis accounting for 40% of cases. Other causes of pancreatitis include alcohol, ERCP induced, medications, metabolic, and idiopathic. Gallstone pancreatitis takes place when a stone impacts and obstructs the ampulla of vater or the pancreatic duct resulting in early activation of exocrine enzymes and auto digestion of the pancreas.  Prognosis is generally good if pancreatitis is mild and appropriately treated. Mortality of mild to moderate gallstone pancreatitis is around 10% which is a decrease in 10-15% over the past 30 years.

Severe pancreatitis is defined by local complications (pseudocyst, hemorrhage, and infection), or signs of organ damage (hypoxia, ARF, DIC, hypocalcemia <7.5). The overall mortality of severe pancreatitis is 30% which has not changed over the past 30 years.

Risk factors for gallstone pancreatitis include: female, advanced age, obesity, multiparous women, high cholesterol, alcoholism, and smoking. 

Most patients have the cardinal symptom of abdominal pain in the epigastric region, but can be in the left or right upper quadrants. Patients usually describe the pain as rapid in onset, constant steady, or boring pain increasing in intensity till it reaches a maximum. When the pain reaches pinnacle with no relief most patients seek medical attention. Patients can present with tachycardia, febrile, and elevation or depression of blood pressure.  This pain can be associated with nausea and emesis and anorexia. Patients can appear jaundiced as obstruction of the ducts causes back up in the biliary system. Most patients on physical exam are tender in the epigastric region and may have a positive Murphy sign.

Pancreatitis should always be in the differential for any patient with upper abdominal pain. The work up for pancreatitis includes cbc, metabolic panel, LFT, and lipase. There is no gold standard diagnosis of pancreatitis most experts agree that lipase is just as sensitive as amylase and has more specificity at 3x normal values. Recently experts in the United Kingdom recommend that lipase should be used for the diagnosis of pancreatitis. Amylase can still be used to diagnose pancreatitis; however it is not as specific at 3x the normal values. ALT above the level of 150IU/L is the most sensitive and specific liver enzyme for gallstone pancreatitis. If pancreatitis is diagnosed ultrasound should be conducted within the first 24 hours to either confirm or rule out gallstones as the cause. CT may also be indicated in severe pancreatitis to rule out peripancreatic complications such as pseudocyst, hemorrhage, and necrosis of pancreas.

Medical management:
Medical management of pancreatitis is usually supportive and tailored to the cause of pancreatitis with emphasis on avoiding complications.  Patients should be admitted to the hospital for intravenous fluids, pain control, antiemetic, and made NPO in the initial phase.  There should be a consult to general surgery for management, ERCP, and cholecystectomy the same hospital admission. Intravenous fluids are the most important intervention in the initial setting, some patients may require up to 6L of fluid as the inflammation leads to sequestration of fluid out of the intravascular space. Give 2-3L bolus of .9ns initially and reassess, if sufficient; place the patient on infusion at 250ml/hr normal saline. Pain control with morphine, no evidence has shown clinical difference or outcome when compared to meperidine.  Nasogastric tube is only indicated in patients with intractable emesis, severe abdominal distention and ileus. Routine use has shown no clinical benefit and has increased the number of days hospitalized. ERCP with sphincterotomy and stone extraction is indicated after the initial pain has subsided and patient clinically improves. This is usually 24-48 hours after admission; early ERCP is only indicated in severe episodes of pancreatitis not responding to conservative management or cholangitis. ERCP may actually induce pancreatitis 5% of the time and is not the definitive treatment for gallstone pancreatitis.  Studies have shown a 30-50% recurrence of gallstone pancreatitis with ERCP alone. Cholecystectomy is the definitive treatment and should be performed on the same hospital admission. Patients with severe pancreatitis require ICU admission.

There are cardiopulmonary, renal, metabolic, infectious, and hematologic complications of pancreatitis. All complications are caused by the inflammatory reaction of pancreatitis. Usually cardiopulmonary collapse due to hypotension or ARDS is the cause of death within the first week. Patients who develop ARDS have a mortality of 50-60% which is the highest of the complications in pancreatitis.

  References
Rosen's Emergency Medicine, seventh edition, 2010, pages 1172-1183, Marx
Tintinalli's Emergency Medicine, sixth edition, 2004, pages 573-577, Tintinalli
Uptodate, Clinical manifestation and diagnosis of acute pancreatitis, 2010, Vege
Pancreatitis, Acute, eMedicine http:emedicine.medscape.com/article/181364
Pancreatitis in Emergency Medicine, eMedicine http://emedicine.medscape.com/article/775867
Dhir, R. et al: Drug-induced pancreatitis: A practical review


03.30.11
by

Intern Report Case Presentation 3.6


Case Presentation by Dr. John Wilburn

Pt. E.R. is a 25 Y.O Hispanic female presenting to the emergency Department with a 4 day history of stomach pain in the periumbilical and epigastric area radiating around the right side to the back.  Patient describes the pain as Constant 8/10 sharp cramping that is aggravated with food and water. Alleviated by sitting up, patient did take Tylenol but it did not help her pain. She reports nausea and has had four episodes of non bloody emesis the night before after eating some bread, the emesis was described as "yellow with food in it". She denies any change in the color or consistency of her bowel movements. LMP was 2 week ago and was a normal cycle. Her abdominal pain has been worsening over the past 4 days and it woke her up from her sleep at 4 am, at which time she decided to seek medical attention.  She denies any trauma or ever having pain like this before. Denies any recent travel and reports that her kids at have had a cold but no GI illnesses. The patient feeling feverish denies any chest pain, shortness of breath or rashes.

ROS:  Negative except as noted per HPI

Past medical history: Denies Diabetes or asthma
Past surgical history: C-section x2
Allergies: Penicillin (rash)
Medication: None
Family history: Father has HTN and Diabetes
Social History: Denies Tobacco, Drinks alcohol socially, denies any illicit drug use. She is currently employed as a waitress and lives at home with her two children ages 3 and 1.

Physical Exam:
VS: 37.5 pulse 106 Bp 128/86 RR 16  99% Room air
General: Laying on her side holding her epigastric area appears uncomfortable but in NAD
HEENT: NC/AT Perrl sclera mildly icteric. EOMI No nasal Discharge no pharyngeal erythema Mucous membranes are dry sublingual has a yellowish color to it.
Neck: Supple No tenderness Trachea is midline. No thyromegaly or Lymphadenopathy
Respiratory: CTAB no W/R/R
Cardiovascular: Tachycardia regular rythm, S1S2 no M/R/G good pulses
Chest: No visible rashes/scars/ no reproducible chest wall tenderness
Abdomen: No lesions or rashes on inspection, Obese, +BS, ST/Tender to Palpation in Epigastric area and RUQ +Murphys sign, No Rebound tenderness, - Rovsings - rigidity. No Guarding.
Extremities: Strength 5/5 b/l upper and Lower ext. Full AROM and PROM palpable radial and dp pulses, SILT and symmetric.
GU: Wnl on inspection no erythema or discharge - No CMT or Adnexal tenderness. Slide shows epithelial cells
Rectal: No Hemorrhoids good tone, no palpable masses. Guaic Negative 

Laboratory Results:
Electrolytes: Na 140, K 3.9, Cl 104, HCO3 24, BUN/Cr 14/0.8, Glucose 125, Ca 8.8
CBC:  Wbc 10.9, H/H 12.3/39.2, Platelets 427
ALT 193, AST 159, Alk Phos 288, Tbili 2.8, Dbili 1.3, Lipase 8005, Amylase 800
Urine hCG: Negative
U/A: 3+bili, 3+ ketones, Sp Gravity 1.025, trace blood, trace LE, Nitrite negative, rbc 2-5
Wbc 5-10, epithelial cells 5-10, trace bacteria 

Ultrasound Demonstrates

  
Questions
  1. Although there is no gold standard for this diagnosis which of the following is considered by most experts to be the most sensitive and specific test available?
    1. CRP
    2. Lipase
    3. Trypsin
    4. Amylase
    5. ALT 
       2.  Which of the of the following Liver Enzymes is the single best marker for biliary     etiology of this diagnosis

a.     ALT
b.     LDH
c.     Total Bilirubin
d.     AST
e.     Alkaline Phosphatase 

  3. Which of the following complications of this diagnosis has the highest mortality?
           
a.     Acute Renal Failure
b.     Myocardial Infarction
c.     Infected Pancreatic Pseudocyst
d.     ARDS
e.     Splenic Vein Thrombosis


4. Which of the following is the definitive treatment?

a.     Cholecystectomy
b.     ERCP
c.     Lexipafant
d.     ERCP with sphincterotomy and stone extraction
e.     Conservative management

Please submit your answers as a comment. Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving's: Intern Report


03.30.11
by

Intern Report Case Presentation 3.6


Case Presentation by Dr. John Wilburn

Pt. E.R. is a 25 Y.O Hispanic female presenting to the emergency Department with a 4 day history of stomach pain in the periumbilical and epigastric area radiating around the right side to the back.  Patient describes the pain as Constant 8/10 sharp cramping that is aggravated with food and water. Alleviated by sitting up, patient did take Tylenol but it did not help her pain. She reports nausea and has had four episodes of non bloody emesis the night before after eating some bread, the emesis was described as "yellow with food in it". She denies any change in the color or consistency of her bowel movements. LMP was 2 week ago and was a normal cycle. Her abdominal pain has been worsening over the past 4 days and it woke her up from her sleep at 4 am, at which time she decided to seek medical attention.  She denies any trauma or ever having pain like this before. Denies any recent travel and reports that her kids at have had a cold but no GI illnesses. The patient feeling feverish denies any chest pain, shortness of breath or rashes.

ROS:  Negative except as noted per HPI

Past medical history: Denies Diabetes or asthma
Past surgical history: C-section x2
Allergies: Penicillin (rash)
Medication: None
Family history: Father has HTN and Diabetes
Social History: Denies Tobacco, Drinks alcohol socially, denies any illicit drug use. She is currently employed as a waitress and lives at home with her two children ages 3 and 1.

Physical Exam:
VS: 37.5 pulse 106 Bp 128/86 RR 16  99% Room air
General: Laying on her side holding her epigastric area appears uncomfortable but in NAD
HEENT: NC/AT Perrl sclera mildly icteric. EOMI No nasal Discharge no pharyngeal erythema Mucous membranes are dry sublingual has a yellowish color to it.
Neck: Supple No tenderness Trachea is midline. No thyromegaly or Lymphadenopathy
Respiratory: CTAB no W/R/R
Cardiovascular: Tachycardia regular rythm, S1S2 no M/R/G good pulses
Chest: No visible rashes/scars/ no reproducible chest wall tenderness
Abdomen: No lesions or rashes on inspection, Obese, +BS, ST/Tender to Palpation in Epigastric area and RUQ +Murphys sign, No Rebound tenderness, - Rovsings - rigidity. No Guarding.
Extremities: Strength 5/5 b/l upper and Lower ext. Full AROM and PROM palpable radial and dp pulses, SILT and symmetric.
GU: Wnl on inspection no erythema or discharge - No CMT or Adnexal tenderness. Slide shows epithelial cells
Rectal: No Hemorrhoids good tone, no palpable masses. Guaic Negative 

Laboratory Results:
Electrolytes: Na 140, K 3.9, Cl 104, HCO3 24, BUN/Cr 14/0.8, Glucose 125, Ca 8.8
CBC:  Wbc 10.9, H/H 12.3/39.2, Platelets 427
ALT 193, AST 159, Alk Phos 288, Tbili 2.8, Dbili 1.3, Lipase 8005, Amylase 800
Urine hCG: Negative
U/A: 3+bili, 3+ ketones, Sp Gravity 1.025, trace blood, trace LE, Nitrite negative, rbc 2-5
Wbc 5-10, epithelial cells 5-10, trace bacteria 

Ultrasound Demonstrates

  
Questions
  1. Although there is no gold standard for this diagnosis which of the following is considered by most experts to be the most sensitive and specific test available?
    1. CRP
    2. Lipase
    3. Trypsin
    4. Amylase
    5. ALT 
       2.  Which of the of the following Liver Enzymes is the single best marker for biliary     etiology of this diagnosis

a.     ALT
b.     LDH
c.     Total Bilirubin
d.     AST
e.     Alkaline Phosphatase 

  3. Which of the following complications of this diagnosis has the highest mortality?
           
a.     Acute Renal Failure
b.     Myocardial Infarction
c.     Infected Pancreatic Pseudocyst
d.     ARDS
e.     Splenic Vein Thrombosis


4. Which of the following is the definitive treatment?

a.     Cholecystectomy
b.     ERCP
c.     Lexipafant
d.     ERCP with sphincterotomy and stone extraction
e.     Conservative management

Please submit your answers as a comment. Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving's: Intern Report


03.25.11
by

Intern Report Case Discussion 3.5


Case Presentation by Dr. Justin Kessler


This patient is suffering from an epidural hematoma with possible transtentorial herniation.  Epidural hematomas are collections of blood between the skull and dura mater.  Epidural hematomas that are large and rapidly expanding are usually caused by arterial bleeding.  Classically these are due to damage of the middle meningeal artery or one of its branches sometimes caused by a temporal bone fracture.  Without swift diagnosis and intervention, patient with arterial epidural hematomas name rapidly deteriorate and die. 

In this patient B.B. underwent initial trauma and was experiencing secondary injury after a "lucid period."  Although lucid intervals only account for proximately 20% of all cases of epidural hematoma the history of a head injury minutes to hours before having declining neurological function are classic for epidural hematomas.  Patient will often still complain of a progressive headache during these lucid intervals as in the case of patient B.B.. 

The pathophysiology lies in the increasing arterial bleed causing increased intracranial pressure.  Because the craniospinal intradural space nonexpandable, some of the volume of brain, CSF, and blood are factors at which if any volume of these components increases the volume of another must decrease to maintain ICP.  This is known as Monroe-Kellie Doctrine.  In the case study, CFS may have been displaced from the intracranial vault to the spinal canal office setting increase of blood volume.  When this compensatory mechanism is overwhelmed and volumes of blood are still increasing the brain matter may start herniate as it too will continue to swell due to congestive brain swelling as well cerebral edema.

On vital sign examination this patient has to have progressive hypertension associated with bradycardia and diminished respiratory effort.  These are specific responses to ICP increase known as the Cushing reflex; usually indicating ICP is that critical levels.

Management ED and this case should include rapid sequence intubation for airway protection since the patient's GCS is 7.  Lidocaine 1.5-2 mg per kilogram IV push may be used to attenuate the cough reflex with intubation since his patient's gag reflex is still intact. 
 Hyperventilation may prevent further herniation in the early phases, hyperventilation works by causing cerebral vasoconstriction.  Onset is within 30 seconds and peaks at 8 minutes after pCO2 drops to arrange of 30-35 mmHg.  However, continued cerebral vasoconstriction also leads to ischemia.
More often hypertonic saline (HTS) is being used to reduce ICP however it is controversial whether it really has an effect.  These studies are using the 3% drip however probably not including the 24% bolus that is given by our cavalier neurointensivists.

Further management to prevent herniation and tissue damage would include osmotic agents such as manitol as well as possible barbiturate coma to decrease metabolic demand of the injured brain tissue. Mannitol at 0.25-1g/kg can effectively reduce ICP and prevent further herniation onset 60minutes and lasting for 6-8hrs. However, with such a large bolus of osmolytes you could overwhelm the kidneys.    Early seizure prophylaxis of benzodiazepines may also be needed, as up to 12% of patients with traumatic brain injury will develop early posttraumatic seizures.  The patient having a depressed skull fracture is indication for acute seizure prophylaxis in his head trauma.

Only after the patient stabilized well CT imaging be required to complete the final diagnosis.

ANSWERS:
#1 Answer: B.) 20% Although Tintinalli's along with was every other study or reference quotes this 20% estimation of the number of the epidural hematomas that will have a heralding lucid interval, if you look back to the original paper below where this estimation came from is actually estimation of 20 up to 50% which has given way to more recent articles stating that the " lucid period" of epidural hematomas is a "classical finding"  when doing a workup for epidural hematomas.
However, one must realize that traumatic brain injury that it comes from many different degrees and levels of injury.  Therefore, a quantifiable estimation based on a study set of patients must be taken with a grain of salt.
I believe the original author accounted for this wide variation by giving a range in his estimation based on data available.  I wrote the question before going to the first source of this statistic sorry.

Liau LM, Bergsneider M, Becker DP. Pathology and pathophysiology of head injury. In: Youmans JR, ed. Neurological Surgery. 4th ed. Philadelphia, Pa: WB Saunders Co; 1996:1549-1594.

#2 Answer: D.) Validated prospective studies have shown that High-risk patients with minor head trauma with any criteria including presence of headache, (mainly a progressive headache), vomiting, age >60, drug or ETOH intoxication, short-term memory deficit, post-traumatic seizures, or evidence of trauma above the clavicals are indicative of increased likelihood of intracranial injuries.  Further high risk factors are also considerations for CT scan which include:

Focal neurologic findingsAsymmetrical pupilsSkull fracture on clinical examinationMultiple traumaSerious, painful, distracting injuriesExternal signs of trauma above the claviclesInitial Glasgow Coma Scale score of 14 or 15Loss of consciousnessPost-traumatic confusion/amnesiaProgressively worsening headacheVomitingPost-traumatic seizureHistory of bleeding disorder/anticoagulationRecent ingestion of intoxicantsUnreliable/unknown history of injuryPrevious neurologic diagnosisPrevious epilepsySuspected child abuseAge >60 yr, <2 yr
- For this reason one could argue that choice (E) may be a likely answer since the child is unable to give an accurate history anyway and might be having a progressive worsening headache, or that the Lady in (C) might be trashed from her two glasses of wine.  The key rebuttal from the author of this question is "might."

#3 Answer : C) GCS<8. The factor that is most predictive of posttraumatic head injury seizures is a GCS<8.  38.7 % of patients in the studies below developed seizures compared with 3.8% of patients with GCS> or equal to 8. Patient age, occipital lobe injury, concomitant use of illicit drugs, and generalized brain injury had not been shown to be predictive of posttraumatic seizures.  Again, every case is different in traumatic brain injury and every study set of patients in different institutions will also be different.  However, this is the data that is available.

Varon J, Marik PE Management of head trauma in children Crit Care Shock 2002;5:133-43.
Varon J, Marik PE Management of  head trauma. Chest Aug 2002 vol.122 669-771

#4 Answer: A&D Ken Norton fought Muhammad Ali in the 1970's however his disability of sounding "punchy" with his speech is due to a TBI from an auto accident.


03.25.11
by

Intern Report Case Discussion 3.5


Case Presentation by Dr. Justin Kessler


This patient is suffering from an epidural hematoma with possible transtentorial herniation.  Epidural hematomas are collections of blood between the skull and dura mater.  Epidural hematomas that are large and rapidly expanding are usually caused by arterial bleeding.  Classically these are due to damage of the middle meningeal artery or one of its branches sometimes caused by a temporal bone fracture.  Without swift diagnosis and intervention, patient with arterial epidural hematomas name rapidly deteriorate and die. 

In this patient B.B. underwent initial trauma and was experiencing secondary injury after a "lucid period."  Although lucid intervals only account for proximately 20% of all cases of epidural hematoma the history of a head injury minutes to hours before having declining neurological function are classic for epidural hematomas.  Patient will often still complain of a progressive headache during these lucid intervals as in the case of patient B.B.. 

The pathophysiology lies in the increasing arterial bleed causing increased intracranial pressure.  Because the craniospinal intradural space nonexpandable, some of the volume of brain, CSF, and blood are factors at which if any volume of these components increases the volume of another must decrease to maintain ICP.  This is known as Monroe-Kellie Doctrine.  In the case study, CFS may have been displaced from the intracranial vault to the spinal canal office setting increase of blood volume.  When this compensatory mechanism is overwhelmed and volumes of blood are still increasing the brain matter may start herniate as it too will continue to swell due to congestive brain swelling as well cerebral edema.

On vital sign examination this patient has to have progressive hypertension associated with bradycardia and diminished respiratory effort.  These are specific responses to ICP increase known as the Cushing reflex; usually indicating ICP is that critical levels.

Management ED and this case should include rapid sequence intubation for airway protection since the patient's GCS is 7.  Lidocaine 1.5-2 mg per kilogram IV push may be used to attenuate the cough reflex with intubation since his patient's gag reflex is still intact. 
 Hyperventilation may prevent further herniation in the early phases, hyperventilation works by causing cerebral vasoconstriction.  Onset is within 30 seconds and peaks at 8 minutes after pCO2 drops to arrange of 30-35 mmHg.  However, continued cerebral vasoconstriction also leads to ischemia.
More often hypertonic saline (HTS) is being used to reduce ICP however it is controversial whether it really has an effect.  These studies are using the 3% drip however probably not including the 24% bolus that is given by our cavalier neurointensivists.

Further management to prevent herniation and tissue damage would include osmotic agents such as manitol as well as possible barbiturate coma to decrease metabolic demand of the injured brain tissue. Mannitol at 0.25-1g/kg can effectively reduce ICP and prevent further herniation onset 60minutes and lasting for 6-8hrs. However, with such a large bolus of osmolytes you could overwhelm the kidneys.    Early seizure prophylaxis of benzodiazepines may also be needed, as up to 12% of patients with traumatic brain injury will develop early posttraumatic seizures.  The patient having a depressed skull fracture is indication for acute seizure prophylaxis in his head trauma.

Only after the patient stabilized well CT imaging be required to complete the final diagnosis.

ANSWERS:
#1 Answer: B.) 20% Although Tintinalli's along with was every other study or reference quotes this 20% estimation of the number of the epidural hematomas that will have a heralding lucid interval, if you look back to the original paper below where this estimation came from is actually estimation of 20 up to 50% which has given way to more recent articles stating that the " lucid period" of epidural hematomas is a "classical finding"  when doing a workup for epidural hematomas.
However, one must realize that traumatic brain injury that it comes from many different degrees and levels of injury.  Therefore, a quantifiable estimation based on a study set of patients must be taken with a grain of salt.
I believe the original author accounted for this wide variation by giving a range in his estimation based on data available.  I wrote the question before going to the first source of this statistic sorry.

Liau LM, Bergsneider M, Becker DP. Pathology and pathophysiology of head injury. In: Youmans JR, ed. Neurological Surgery. 4th ed. Philadelphia, Pa: WB Saunders Co; 1996:1549-1594.

#2 Answer: D.) Validated prospective studies have shown that High-risk patients with minor head trauma with any criteria including presence of headache, (mainly a progressive headache), vomiting, age >60, drug or ETOH intoxication, short-term memory deficit, post-traumatic seizures, or evidence of trauma above the clavicals are indicative of increased likelihood of intracranial injuries.  Further high risk factors are also considerations for CT scan which include:

Focal neurologic findingsAsymmetrical pupilsSkull fracture on clinical examinationMultiple traumaSerious, painful, distracting injuriesExternal signs of trauma above the claviclesInitial Glasgow Coma Scale score of 14 or 15Loss of consciousnessPost-traumatic confusion/amnesiaProgressively worsening headacheVomitingPost-traumatic seizureHistory of bleeding disorder/anticoagulationRecent ingestion of intoxicantsUnreliable/unknown history of injuryPrevious neurologic diagnosisPrevious epilepsySuspected child abuseAge >60 yr, <2 yr
- For this reason one could argue that choice (E) may be a likely answer since the child is unable to give an accurate history anyway and might be having a progressive worsening headache, or that the Lady in (C) might be trashed from her two glasses of wine.  The key rebuttal from the author of this question is "might."

#3 Answer : C) GCS<8. The factor that is most predictive of posttraumatic head injury seizures is a GCS<8.  38.7 % of patients in the studies below developed seizures compared with 3.8% of patients with GCS> or equal to 8. Patient age, occipital lobe injury, concomitant use of illicit drugs, and generalized brain injury had not been shown to be predictive of posttraumatic seizures.  Again, every case is different in traumatic brain injury and every study set of patients in different institutions will also be different.  However, this is the data that is available.

Varon J, Marik PE Management of head trauma in children Crit Care Shock 2002;5:133-43.
Varon J, Marik PE Management of  head trauma. Chest Aug 2002 vol.122 669-771

#4 Answer: A&D Ken Norton fought Muhammad Ali in the 1970's however his disability of sounding "punchy" with his speech is due to a TBI from an auto accident.


03.22.11
by

Intern Report Case Presentation 3.5


Case Presentation by Dr. Justin Kessler


Patient B.B. a 17-year-old high school football player presenting to the emergency department via EMS after collapsing to the ground unresponsive approximately 3 hours after being struck in the head without a helmet on by another player's helmet. Initially he was dazed but was able to stand up and joke about what a "hard head he had." He complained of a headache throughout the rest of practice and vomited once per his coach who thought it was due to the heat. PMHx significant only for acne. Patient takes Tylenol for headaches PRN after football practice. On exam patient is not responsive to name, he makes gurgling mumbles, slowly opens his eyes to painful stimuli, and only has an abnormal flexed posture does not withdraw to pain.

Physical Exam:

Vitals: BP146/92, HR 98 , RR9, Sat87% Room, Temp 37.4

HEENT: HEAD: Slight boney stepoff along the patient's right temporal area. No Scalp Lacerations.
EYES: The pupils are 7mmOD 3mm OS sluggish reactive to light,. fundoscopic exam shows evidence of swelling of optic disk ,hyperma, and loss of physiologic cupping on exam in OD only. Sclera were anicteric, conjunctiva were without palor.
EARS: Pinnae are intact bilaterally, TM are clear,no evidence of hemotympanum Bilaterally.
NOSE: No noticeable deformity, moist mucosa, no erythema, no epistaxis, discharge, no swollen turbinates.
MOUTH AND THROAT: Mucous membranes are moist,no erythema, no tonsillar exudates, no intraoral leisions of the gums, tongue, lips, or palates.
CV: S1 S2 present, regular rhythm and tachycardic rate~ 100bpm, no murmurs
Resp: Slow shallow breaths,
Abd: Soft, nondistended, BS all 4 Qs
Ext: Peripheral pulses present in all 4 limbs, cap refill <2 seconds ROM intact with passive movement of all 4 limbs. Tone increased.
Back: No tenderness to palpation throughout cervical, thoracic, and lumbar spine. No bony deformity, crepitus, or step-offs noted.
Neuro: Pt obtunded, Decorticate posturing, not opening eyes to command or name. Positive gag reflex. Absent ankle jerk bilaterally, Babinski negative bilaterally.

Lab Results: 
Electrolytes, BUN, creatinine, glucose, and CBC were all within normal limits.
NORMAL ECG
12-lead ECG performed at 1550 is interpreted as revealing tachycardic normal sinus rhythm at a rate of 102 beats per minute. Axis was normal. There were no ST or T wave abnormalities to suggest myocardial ischemia or injury.

Diagnostic Studies: Head CT as Follows:



Questions

1. Following Injury in which there is later radiographic evidence on head CT of an epidural hematoma what is the estimated percentage in which there is a "lucid" period before deterioration?
A. 75%
B. 60%
C. 20%
D. 15%
E.  5%


2. In regards to a Minor Head Trauma which of the following patients would warrant CT scanof head  or prolonged emergency department observation?
A. A 23 YO male that bumped his head on a door 2 days ago, currently asymptomatic, no LOC with intact orientation, memory.
B. A 30 YO male with a minor headache after being hit in the head from a falling telephone book(for Kansas City), no vomiting no LOC
C. A 45 YO female with fall to carpeted surface wearing high heels after drinking 2 glasses of wine with no change in consciousness, intact orientation and recall.
D.A 61 YO male who tripped over a shopping cart hit head into a car door with past history of epilepsy, last seizure was >20 years ago.
E. 5 YO female running away from her brother that hit her head on a coffee table complains of headache, witnessed by mother, child consolable on scene.


3.Which of the following factors has the greatest predictive value in the Development of seizures following head trauma?
A Patient Age
B. Occipial Lobe injury
C. Glasgow coma Score <8
D. Concomitant use of  illicit drugs
E generalized brain injury.


4.Two of these Famous TBI patients are related other than the fact that they had Traumatic Brain injury which two?

A.Ken Norton
B.Ellen White
C.Natasha Richardson
D.Muhammad Ali
E.Larry Flynt
F.Phineas Gage



Please submit your answers as a comment. Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving's: Intern Report


03.22.11
by

Intern Report Case Presentation 3.5


Case Presentation by Dr. Justin Kessler


Patient B.B. a 17-year-old high school football player presenting to the emergency department via EMS after collapsing to the ground unresponsive approximately 3 hours after being struck in the head without a helmet on by another player's helmet. Initially he was dazed but was able to stand up and joke about what a "hard head he had." He complained of a headache throughout the rest of practice and vomited once per his coach who thought it was due to the heat. PMHx significant only for acne. Patient takes Tylenol for headaches PRN after football practice. On exam patient is not responsive to name, he makes gurgling mumbles, slowly opens his eyes to painful stimuli, and only has an abnormal flexed posture does not withdraw to pain.

Physical Exam:

Vitals: BP146/92, HR 98 , RR9, Sat87% Room, Temp 37.4

HEENT: HEAD: Slight boney stepoff along the patient's right temporal area. No Scalp Lacerations.
EYES: The pupils are 7mmOD 3mm OS sluggish reactive to light,. fundoscopic exam shows evidence of swelling of optic disk ,hyperma, and loss of physiologic cupping on exam in OD only. Sclera were anicteric, conjunctiva were without palor.
EARS: Pinnae are intact bilaterally, TM are clear,no evidence of hemotympanum Bilaterally.
NOSE: No noticeable deformity, moist mucosa, no erythema, no epistaxis, discharge, no swollen turbinates.
MOUTH AND THROAT: Mucous membranes are moist,no erythema, no tonsillar exudates, no intraoral leisions of the gums, tongue, lips, or palates.
CV: S1 S2 present, regular rhythm and tachycardic rate~ 100bpm, no murmurs
Resp: Slow shallow breaths,
Abd: Soft, nondistended, BS all 4 Qs
Ext: Peripheral pulses present in all 4 limbs, cap refill <2 seconds ROM intact with passive movement of all 4 limbs. Tone increased.
Back: No tenderness to palpation throughout cervical, thoracic, and lumbar spine. No bony deformity, crepitus, or step-offs noted.
Neuro: Pt obtunded, Decorticate posturing, not opening eyes to command or name. Positive gag reflex. Absent ankle jerk bilaterally, Babinski negative bilaterally.

Lab Results: 
Electrolytes, BUN, creatinine, glucose, and CBC were all within normal limits.
NORMAL ECG
12-lead ECG performed at 1550 is interpreted as revealing tachycardic normal sinus rhythm at a rate of 102 beats per minute. Axis was normal. There were no ST or T wave abnormalities to suggest myocardial ischemia or injury.

Diagnostic Studies: Head CT as Follows:



Questions

1. Following Injury in which there is later radiographic evidence on head CT of an epidural hematoma what is the estimated percentage in which there is a "lucid" period before deterioration?
A. 75%
B. 60%
C. 20%
D. 15%
E.  5%


2. In regards to a Minor Head Trauma which of the following patients would warrant CT scanof head  or prolonged emergency department observation?
A. A 23 YO male that bumped his head on a door 2 days ago, currently asymptomatic, no LOC with intact orientation, memory.
B. A 30 YO male with a minor headache after being hit in the head from a falling telephone book(for Kansas City), no vomiting no LOC
C. A 45 YO female with fall to carpeted surface wearing high heels after drinking 2 glasses of wine with no change in consciousness, intact orientation and recall.
D.A 61 YO male who tripped over a shopping cart hit head into a car door with past history of epilepsy, last seizure was >20 years ago.
E. 5 YO female running away from her brother that hit her head on a coffee table complains of headache, witnessed by mother, child consolable on scene.


3.Which of the following factors has the greatest predictive value in the Development of seizures following head trauma?
A Patient Age
B. Occipial Lobe injury
C. Glasgow coma Score <8
D. Concomitant use of  illicit drugs
E generalized brain injury.


4.Two of these Famous TBI patients are related other than the fact that they had Traumatic Brain injury which two?

A.Ken Norton
B.Ellen White
C.Natasha Richardson
D.Muhammad Ali
E.Larry Flynt
F.Phineas Gage



Please submit your answers as a comment. Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving's: Intern Report


03.22.11
by

Intern Report Case Discussion 3.4


Case Presentation by Dr. Kevin Sprague



The patient is suffering from acute cholecystitis. This is caused by inflammation of the gallbladder, most commonly after a gallstone (cholelithiasis) obstructs the neck of the gallbladder or cystic duct. The obstruction causes mucus layer disruption, irritation and inflammation, which leads to dysmotility and distention. This inflammation occurs in the absence of bacterial infection. The most common type of gallstones in western civilization are cholesterol stones which occur when the cholesterol in the gallbladder exceeds the solubilizing capacity. The cholesterol will then nucleate into monohydrate crystals. These crystals cause gallbladder hypomotility which further accelerates cholesterol stone formation.

Cholesterol stones account for approximately 80% of gallstones in western civilization. The other type are designated pigment stones. These stones are a mixture of abnormal insoluble calcium salts of unconjugated bilirubin along with inorganic calcium salts. The amount of unconjugated bilirubin increases with infection of the biliary tract, and so infection with E. Coli or Ascaris lumbricoides (roundworm) increases the likelihood of pigment stone formation. These stones are radiopaque once the concentration of Ca exceeds 4%.

2-12% of cases are not caused by gallstones and are classified as acalculous. These typically occur in severely ill patients. Common scenarios are: postoperative state after major surgery, severe trauma, severe burns, multisystem organ failure, and sepsis. Diagnosing these patients is much more difficult as the onset is insidious and symptoms are obscured by the previously mentioned scenarios. The incidence of gangrene and perforation are higher in these patients. The mortality rate from acalculous cholecystitis is as high as 41%.

A differential for acute cholecystitis can include hepatitis, hepatic abscess, pyelonephritis, RLL pneumonia/pleurisy, perforated duodenal ulcer, pancreatitis, and appendicitis. Patients may have a mild fever, anorexia, nausea, vomiting, tachycardia, and diaphoresis. They may have had previous episodes of biliary pain. WBC count is normal in 27-40% of patients. Alkaline phosphatase, bilirubin, and serum aminotransferase are often within normal limits, but may be mildly elevated.

Ultrasound imaging is most commonly used in the ED as it is rapid and has good sensitivity. A gallstone or sludge may be visualized as well as gallbladder distention, gallbladder wall thickening, and pericholecystic fluid. A positive sonographic Murphy's sign has good specificity for cholecystitis.

Treatment includes basic supportive measures, correcting fluid status and electrolyte imbalance. Emesis is managed with antiemetics and nasogastric suction. NG suction may diminish biliary secretion and excretion. Pain control may be achieved with narcotics. Antibiotics should be administered to prevent ascending infection. For uncomplicated cases, a 2nd or 3rd generation cephalosporin is recommended.

Common complications are gangrene, necrosis, and perforation. Emphysematous cholecystitis occurs in 1% of cases. This is the consequence of gas producing organisms (E. Coli, Klebsiella, C. perfringens) invading the mucosa of the gallbladder.


Answers

D. Hepatobiliary Iminodiacetic Acid (HIDA) Scan is the most sensitive at 97% for acute cholecystitis. Ultrasound is a close second at 94% sensitive. According to Rosen's Emergency Medicine 7th Edition, CT may be 92% sensitive. However, I have also seen it reported as low as 50% sensitive. The bottom line is that CT is a much less preferable imaging modality. X-Ray will pick up 10% of gallstones, or about half of the cases of pigmented stones. I have never seen any information on MRI for acute cholecystitis, but I needed a 5th option.

E. This is sort of a cheap question. Over 90% of cases are caused by mechanical obstruction of the gallbladder neck or cystic duct by a gallstone. Even though the etiology is noninfectious, antibiotic therapy with a 2nd or 3rd generation cephalosporin is recommended. The other 4 choices are the organisms most commonly responsible for ascending cholangitis.

B. Porcelain Gallbladder is caused by calcifications within the gallbladder wall. The gallbladder may be palpable through the skin (Courvoisier's sign). There is a high incidence of gallbladder carcinoma associated with this radiologic finding. These patients should be referred for a cholecystectomy.


03.22.11
by

Intern Report Case Discussion 3.4


Case Presentation by Dr. Kevin Sprague



The patient is suffering from acute cholecystitis. This is caused by inflammation of the gallbladder, most commonly after a gallstone (cholelithiasis) obstructs the neck of the gallbladder or cystic duct. The obstruction causes mucus layer disruption, irritation and inflammation, which leads to dysmotility and distention. This inflammation occurs in the absence of bacterial infection. The most common type of gallstones in western civilization are cholesterol stones which occur when the cholesterol in the gallbladder exceeds the solubilizing capacity. The cholesterol will then nucleate into monohydrate crystals. These crystals cause gallbladder hypomotility which further accelerates cholesterol stone formation.

Cholesterol stones account for approximately 80% of gallstones in western civilization. The other type are designated pigment stones. These stones are a mixture of abnormal insoluble calcium salts of unconjugated bilirubin along with inorganic calcium salts. The amount of unconjugated bilirubin increases with infection of the biliary tract, and so infection with E. Coli or Ascaris lumbricoides (roundworm) increases the likelihood of pigment stone formation. These stones are radiopaque once the concentration of Ca exceeds 4%.

2-12% of cases are not caused by gallstones and are classified as acalculous. These typically occur in severely ill patients. Common scenarios are: postoperative state after major surgery, severe trauma, severe burns, multisystem organ failure, and sepsis. Diagnosing these patients is much more difficult as the onset is insidious and symptoms are obscured by the previously mentioned scenarios. The incidence of gangrene and perforation are higher in these patients. The mortality rate from acalculous cholecystitis is as high as 41%.

A differential for acute cholecystitis can include hepatitis, hepatic abscess, pyelonephritis, RLL pneumonia/pleurisy, perforated duodenal ulcer, pancreatitis, and appendicitis. Patients may have a mild fever, anorexia, nausea, vomiting, tachycardia, and diaphoresis. They may have had previous episodes of biliary pain. WBC count is normal in 27-40% of patients. Alkaline phosphatase, bilirubin, and serum aminotransferase are often within normal limits, but may be mildly elevated.

Ultrasound imaging is most commonly used in the ED as it is rapid and has good sensitivity. A gallstone or sludge may be visualized as well as gallbladder distention, gallbladder wall thickening, and pericholecystic fluid. A positive sonographic Murphy's sign has good specificity for cholecystitis.

Treatment includes basic supportive measures, correcting fluid status and electrolyte imbalance. Emesis is managed with antiemetics and nasogastric suction. NG suction may diminish biliary secretion and excretion. Pain control may be achieved with narcotics. Antibiotics should be administered to prevent ascending infection. For uncomplicated cases, a 2nd or 3rd generation cephalosporin is recommended.

Common complications are gangrene, necrosis, and perforation. Emphysematous cholecystitis occurs in 1% of cases. This is the consequence of gas producing organisms (E. Coli, Klebsiella, C. perfringens) invading the mucosa of the gallbladder.


Answers

D. Hepatobiliary Iminodiacetic Acid (HIDA) Scan is the most sensitive at 97% for acute cholecystitis. Ultrasound is a close second at 94% sensitive. According to Rosen's Emergency Medicine 7th Edition, CT may be 92% sensitive. However, I have also seen it reported as low as 50% sensitive. The bottom line is that CT is a much less preferable imaging modality. X-Ray will pick up 10% of gallstones, or about half of the cases of pigmented stones. I have never seen any information on MRI for acute cholecystitis, but I needed a 5th option.

E. This is sort of a cheap question. Over 90% of cases are caused by mechanical obstruction of the gallbladder neck or cystic duct by a gallstone. Even though the etiology is noninfectious, antibiotic therapy with a 2nd or 3rd generation cephalosporin is recommended. The other 4 choices are the organisms most commonly responsible for ascending cholangitis.

B. Porcelain Gallbladder is caused by calcifications within the gallbladder wall. The gallbladder may be palpable through the skin (Courvoisier's sign). There is a high incidence of gallbladder carcinoma associated with this radiologic finding. These patients should be referred for a cholecystectomy.


03.17.11
by

Intern Report Case Presentation 3.4


Case Presentation by Dr. Kevin Sprague


An otherwise healthy 42 year old female presents to the Emergency Department complaining of 4 hours of constant epigastric pain and vomiting that began 30 minutes after eating lunch.  The pain is sharp, constant, radiates to her shoulder blade, and is 8/10 in severity.  She has been unable to hold any food or liquid since the vomiting began.  She has vomited 3 times  She denies hematemesis.  She is concerned this is food poisoning.  She states she has never had this happen before.  However, she has had some episodes of mild abdominal sharp pain after eating that resolved after roughly an hour.  After she gives you the history, she vomits yellow liquid in a basin before your eyes.

Physical Exam
Vitals: Temp 38.2, BP 128/62, HR 108, RR 20, Sat 99% on RA
General: Uncomfortable, in no acute respiratory distress
Lungs: CTAB
Cardiac: S1S2, RRR, tachycardic rate, normal rhythm
Abdomen: RUQ tenderness, involuntary guarding, rebound tenderness, normal bowel sounds throughout the abdomen
Otherwise normal physical exam

EKG demonstrates a tachycardic sinus rhythm.  Chest X-Ray is negative for any acute process.  WBC is mildly elevated at 13.4.  The rest of the CBC, electrolytes, U/A, AST/ALT, alk phos, lipase, bilirubin are within normal limits.

You obtain an ultrasound which demonstrates the following.

Questions

1.  What is the most sensitive test for cholecystitis?
  1. X-Ray
  2. Ultrasound
  3. CT
  4. HIDA scan
  5. MRI
2.  Which infectious agent causes the majority of cholecystitis in the United States?
  1. E. Coli
  2. Klebsiella
  3. Enterococcus
  4. Bacteriodes
  5. No infectious etiology
3.  Porcelain Gallbladder is associated with which of the following?
  1. Primary hyperparathyroidism
  2. Carcinoma
  3. Ascending cholangitis
  4. Paget's disease
  5. Hypercholesterolemia
Please submit your answers as a comment. Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving's: Intern Report


03.17.11
by

Intern Report Case Presentation 3.4


Case Presentation by Dr. Kevin Sprague


An otherwise healthy 42 year old female presents to the Emergency Department complaining of 4 hours of constant epigastric pain and vomiting that began 30 minutes after eating lunch.  The pain is sharp, constant, radiates to her shoulder blade, and is 8/10 in severity.  She has been unable to hold any food or liquid since the vomiting began.  She has vomited 3 times  She denies hematemesis.  She is concerned this is food poisoning.  She states she has never had this happen before.  However, she has had some episodes of mild abdominal sharp pain after eating that resolved after roughly an hour.  After she gives you the history, she vomits yellow liquid in a basin before your eyes.

Physical Exam
Vitals: Temp 38.2, BP 128/62, HR 108, RR 20, Sat 99% on RA
General: Uncomfortable, in no acute respiratory distress
Lungs: CTAB
Cardiac: S1S2, RRR, tachycardic rate, normal rhythm
Abdomen: RUQ tenderness, involuntary guarding, rebound tenderness, normal bowel sounds throughout the abdomen
Otherwise normal physical exam

EKG demonstrates a tachycardic sinus rhythm.  Chest X-Ray is negative for any acute process.  WBC is mildly elevated at 13.4.  The rest of the CBC, electrolytes, U/A, AST/ALT, alk phos, lipase, bilirubin are within normal limits.

You obtain an ultrasound which demonstrates the following.

Questions

1.  What is the most sensitive test for cholecystitis?
  1. X-Ray
  2. Ultrasound
  3. CT
  4. HIDA scan
  5. MRI
2.  Which infectious agent causes the majority of cholecystitis in the United States?
  1. E. Coli
  2. Klebsiella
  3. Enterococcus
  4. Bacteriodes
  5. No infectious etiology
3.  Porcelain Gallbladder is associated with which of the following?
  1. Primary hyperparathyroidism
  2. Carcinoma
  3. Ascending cholangitis
  4. Paget's disease
  5. Hypercholesterolemia
Please submit your answers as a comment. Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving's: Intern Report


03.13.11
by

Intern Report Case Discussion 3.3


Case Presentation by Dr. Ryan Doss



This patient is suffering from acute chest syndrome, a complication of sickle cell disease and currently the leading cause of death in patients with SCD in the United States (with a total mortality in adults of 9%).  As we all know, in sickle cell disease the sickling of red blood cells is precipitated by hypoxia. Any condition which results in a relative hypoxia in the pulmonary microvasculature can thus cause an attack localized to the lungs (or of course distributed more diffusely). 

ACS is more common but less deadly in the pediatric age group, especially ages 2-4, and the incidence gradually decreases with age.  In younger patients an attack of acute chest syndrome is most often brought on by an infection with viruses or bacteria. Fat microembolization from marrow necrosis - itself a complication of a more generalized sickle cell crisis - is more common in adults. Some other causes include asthma, atelectasis from splinting secondary to rib pain, or iatrogenic fluid overload/opiate-induced respiratory depression.

Given his age we can speculate that this patient's ACS is caused by either a fat embolus from his days-long sickle cell crisis or atelectasis from his right lower rib cage infarction. Practically, however, it doesn't really matter what caused his current condition. The management of ACS from any cause involves supportive care, empiric antibiotics, and exchange transfusion.

Aggressive pain control and oxygenation serve to reduce the sickling of the patient's RBCs by decreasing splinting, improving tidal volume, and helping to reduce the localized hypoxemia. Pulse oximetry will probably be inaccurate but can be useful as an approximation. A reading on room air below 92% should be evaluated more fully with an ABG. Calculation of the A-a gradient helps guide the disposition. There are no agreed-upon standards, but in general an elevated A-a gradient or a rapid rise in the gradient should steer the ED physician toward intubation and ICU admission. Inhaled bronchodilator therapy may be helpful, especially if the patient has a history of asthma.

Empiric antibiotics should include coverage for Chlamydia pneumoniae, Mycoplasma pneumoniae, and Streptococcus pneumoniae, the three most commonly encountered bacteria in infectious ACS (with Chlamydia pnemoniae being most common). This would involve a third-generation cephalosporin paired with a macrolide or quinolone.

Simple transfusion of 2-4u PRBCs should be considered early after the diagnosis of ACS. This appears to be as effective as exchange transfusion unless the patient's clinical condition is more severe. It is important to maintain a Hb below 10 mg/dL because higher Hb levels can cause hyperviscosity in the microvasculature in sickle cell patients. This is not normally a concern with simple transfusion due to the sickle cell crisis patient's acute drop in Hb.

Answers

1. As discussed above, calculation of the A-a gradient is an important management tool for the patient with moderate-severe ACS. But nobody wants to do that, including me, because math is hard. Especially when you have a patient in front of you with chest pain struggling to breathe. So let's take this a step at a time. (Or skip ahead to the end of this question if you just want to memorize the equation which is totally cool but cowardly).

First: the A-a gradient is simply the difference between the oxygen in the alveoli and the oxygen in the artery. We know the pressure of oxygen in the artery from the ABG measurement (81). There we're halfway done! (Not really).

The second half involves calculating the pressure of oxygen in the alveoli. Let's start by assuming we're at about sea level and the barometric pressure is 760mmHg. Multiply that by the room air FIO2 (21%, duh) and we have our oxygen pressure (159.6 or 160).

Unfortunately, we can't just use the calculated pressure of oxygen in the surrounding atmosphere. First of all, the pressure of oxygen in the air we inspire changes on its way through our respiratory tract. This is because the atmosphere becomes more humid as the air enters our body. The water vapor pressure (47mmHg) needs to be subtracted from the atmosphere's barometric pressure. Wait...why would we subtract water vapor pressure from barometric pressure? It seems like we should be adding it. BUT the molecular mass of water vapor is actually lower than that of dry air. Ok, crap, rewind and subtract 47 from 760 to get 719. Now 719 x .21 = 150.99 or 151.

If you're still reading at this point, I love you. And I'm sorry because it's about to get a whole lot worse.

Ok so the alveolar pressure of oxygen is 151! Now let's just compare that to the oxygen in the arteries! NO, you FOOL. When we measure the arterial pressure of oxygen we are measuring the oxygen left over in the artery AFTER the tissues take what they need. We don't want to compare the oxygen in the alveoli to the oxygen in the artery AFTER the body uses what it needs. We want to compare the gradient at the exact moment they straddle the air/blood barrier. So we need to add the oxygen the body consumed back into the arterial oxygen reading. OR we need to subtract it from the PIO2. Either way. Whoever wrote down the alveolar gas equation did it the second way since it's less intuitive (hooray...).

The respiratory quotient is a number derived by experimentation (for completely unrelated reasons...namely to calculate BMR based on different types of caloric intake) which equates to (CO2 eliminated/O2 consumed). It is a constant (for our purposes) and this constant is 0.8. So we just need to know CO2 eliminated and we'll know our O2 consumed, which we can then add back into our PaO2. If you think about it we kind of already know our CO2 eliminated, because we measured the CO2 in our artery with the ABG and our body HAS to get rid of all of that or we'll just steadily accumulate CO2 until we die. The PaCO2 in our ABG is 31. Rearrange (R=CO2 eliminated/O2 consumed) and you get (O2 consumed = CO2 eliminated/R or 31/0.8 or 38.75 or 39).

Oh god we're getting so close. Now add our O2 consumed (39) back to our measured PaO2 (81) to get 120. Subtract 120 from our calculated PAO2 (151) to get 31! Normal is less than 10. This guy is screwed.

Or you could memorize (150 - PaCO2/0.8) - PaO2. Whichever you prefer.

Er...P.S. The alveolar gas equation is PAO2 = FIO2(Patm - PH2O) - (PaCO2/R)

Answer: B

2. I don't really have a long-winded explanation for this one. According to Principles of Critical Care, neurologic complications including seizure and stroke are the most common complications of acute chest syndrome. Cardiac, gastrointestinal, and renal complications are infrequent.

Answer: C

3. Again, no big explanation here. This is just experimentally determined as far as I know. If anybody has a hypothetical explanation I'd be very interested in hearing it.

Answer: A

4. So a lot of these would be useful in some way, and arguments could be made for each. I'll skip over A and D and E as they don't involve any treatment (well, not any scientifically proven treatment anyway) and presumably you'd be most interested in treatment.
Answer C could be useful to decrease splinting and increase oxygenation. Plus with a 9% mortality and no REAL effective medical treatment you might as well go out with a smile on your face.
Answer B is a devious misdirection. Phlogisticated (i.e. gaseous) laughing anesthetic is nitrous oxide (N2O). According to Tintinalli's, "Inhaled nitric oxide has shown benefit in the management of acute chest syndrome, apparently due to its vasodilatory effects that improves the coordination between ventilation and perfusion in the damaged lung regions with minimal systemic absorption. In addition nitric oxide reduces adhesion of RBCs and leukocytes to endothelial cells by decreasing the activity of vascular cell adhesion molecule-1." But of course the chemical formula for nitric oxide is NO and not N2O! HAHAHA you fools! To my knowledge nitrous oxide does not have the useful vasodilatory effects nitric oxide does in the treatment of ACS. While it might be useful in the same sense that heroin would be (anesthesia) you would be decreasing your FIO2 by displacing O2 with another gas. Then again, chugging a bottle of baby heroin would presumably decrease your respiratory drive so I guess you can feel free to pick your poison.

In light of this snap reconsideration, I will accept both B and C.



03.13.11
by

Intern Report Case Discussion 3.3


Case Presentation by Dr. Ryan Doss



This patient is suffering from acute chest syndrome, a complication of sickle cell disease and currently the leading cause of death in patients with SCD in the United States (with a total mortality in adults of 9%).  As we all know, in sickle cell disease the sickling of red blood cells is precipitated by hypoxia. Any condition which results in a relative hypoxia in the pulmonary microvasculature can thus cause an attack localized to the lungs (or of course distributed more diffusely). 

ACS is more common but less deadly in the pediatric age group, especially ages 2-4, and the incidence gradually decreases with age.  In younger patients an attack of acute chest syndrome is most often brought on by an infection with viruses or bacteria. Fat microembolization from marrow necrosis - itself a complication of a more generalized sickle cell crisis - is more common in adults. Some other causes include asthma, atelectasis from splinting secondary to rib pain, or iatrogenic fluid overload/opiate-induced respiratory depression.

Given his age we can speculate that this patient's ACS is caused by either a fat embolus from his days-long sickle cell crisis or atelectasis from his right lower rib cage infarction. Practically, however, it doesn't really matter what caused his current condition. The management of ACS from any cause involves supportive care, empiric antibiotics, and exchange transfusion.

Aggressive pain control and oxygenation serve to reduce the sickling of the patient's RBCs by decreasing splinting, improving tidal volume, and helping to reduce the localized hypoxemia. Pulse oximetry will probably be inaccurate but can be useful as an approximation. A reading on room air below 92% should be evaluated more fully with an ABG. Calculation of the A-a gradient helps guide the disposition. There are no agreed-upon standards, but in general an elevated A-a gradient or a rapid rise in the gradient should steer the ED physician toward intubation and ICU admission. Inhaled bronchodilator therapy may be helpful, especially if the patient has a history of asthma.

Empiric antibiotics should include coverage for Chlamydia pneumoniae, Mycoplasma pneumoniae, and Streptococcus pneumoniae, the three most commonly encountered bacteria in infectious ACS (with Chlamydia pnemoniae being most common). This would involve a third-generation cephalosporin paired with a macrolide or quinolone.

Simple transfusion of 2-4u PRBCs should be considered early after the diagnosis of ACS. This appears to be as effective as exchange transfusion unless the patient's clinical condition is more severe. It is important to maintain a Hb below 10 mg/dL because higher Hb levels can cause hyperviscosity in the microvasculature in sickle cell patients. This is not normally a concern with simple transfusion due to the sickle cell crisis patient's acute drop in Hb.

Answers

1. As discussed above, calculation of the A-a gradient is an important management tool for the patient with moderate-severe ACS. But nobody wants to do that, including me, because math is hard. Especially when you have a patient in front of you with chest pain struggling to breathe. So let's take this a step at a time. (Or skip ahead to the end of this question if you just want to memorize the equation which is totally cool but cowardly).

First: the A-a gradient is simply the difference between the oxygen in the alveoli and the oxygen in the artery. We know the pressure of oxygen in the artery from the ABG measurement (81). There we're halfway done! (Not really).

The second half involves calculating the pressure of oxygen in the alveoli. Let's start by assuming we're at about sea level and the barometric pressure is 760mmHg. Multiply that by the room air FIO2 (21%, duh) and we have our oxygen pressure (159.6 or 160).

Unfortunately, we can't just use the calculated pressure of oxygen in the surrounding atmosphere. First of all, the pressure of oxygen in the air we inspire changes on its way through our respiratory tract. This is because the atmosphere becomes more humid as the air enters our body. The water vapor pressure (47mmHg) needs to be subtracted from the atmosphere's barometric pressure. Wait...why would we subtract water vapor pressure from barometric pressure? It seems like we should be adding it. BUT the molecular mass of water vapor is actually lower than that of dry air. Ok, crap, rewind and subtract 47 from 760 to get 719. Now 719 x .21 = 150.99 or 151.

If you're still reading at this point, I love you. And I'm sorry because it's about to get a whole lot worse.

Ok so the alveolar pressure of oxygen is 151! Now let's just compare that to the oxygen in the arteries! NO, you FOOL. When we measure the arterial pressure of oxygen we are measuring the oxygen left over in the artery AFTER the tissues take what they need. We don't want to compare the oxygen in the alveoli to the oxygen in the artery AFTER the body uses what it needs. We want to compare the gradient at the exact moment they straddle the air/blood barrier. So we need to add the oxygen the body consumed back into the arterial oxygen reading. OR we need to subtract it from the PIO2. Either way. Whoever wrote down the alveolar gas equation did it the second way since it's less intuitive (hooray...).

The respiratory quotient is a number derived by experimentation (for completely unrelated reasons...namely to calculate BMR based on different types of caloric intake) which equates to (CO2 eliminated/O2 consumed). It is a constant (for our purposes) and this constant is 0.8. So we just need to know CO2 eliminated and we'll know our O2 consumed, which we can then add back into our PaO2. If you think about it we kind of already know our CO2 eliminated, because we measured the CO2 in our artery with the ABG and our body HAS to get rid of all of that or we'll just steadily accumulate CO2 until we die. The PaCO2 in our ABG is 31. Rearrange (R=CO2 eliminated/O2 consumed) and you get (O2 consumed = CO2 eliminated/R or 31/0.8 or 38.75 or 39).

Oh god we're getting so close. Now add our O2 consumed (39) back to our measured PaO2 (81) to get 120. Subtract 120 from our calculated PAO2 (151) to get 31! Normal is less than 10. This guy is screwed.

Or you could memorize (150 - PaCO2/0.8) - PaO2. Whichever you prefer.

Er...P.S. The alveolar gas equation is PAO2 = FIO2(Patm - PH2O) - (PaCO2/R)

Answer: B

2. I don't really have a long-winded explanation for this one. According to Principles of Critical Care, neurologic complications including seizure and stroke are the most common complications of acute chest syndrome. Cardiac, gastrointestinal, and renal complications are infrequent.

Answer: C

3. Again, no big explanation here. This is just experimentally determined as far as I know. If anybody has a hypothetical explanation I'd be very interested in hearing it.

Answer: A

4. So a lot of these would be useful in some way, and arguments could be made for each. I'll skip over A and D and E as they don't involve any treatment (well, not any scientifically proven treatment anyway) and presumably you'd be most interested in treatment.
Answer C could be useful to decrease splinting and increase oxygenation. Plus with a 9% mortality and no REAL effective medical treatment you might as well go out with a smile on your face.
Answer B is a devious misdirection. Phlogisticated (i.e. gaseous) laughing anesthetic is nitrous oxide (N2O). According to Tintinalli's, "Inhaled nitric oxide has shown benefit in the management of acute chest syndrome, apparently due to its vasodilatory effects that improves the coordination between ventilation and perfusion in the damaged lung regions with minimal systemic absorption. In addition nitric oxide reduces adhesion of RBCs and leukocytes to endothelial cells by decreasing the activity of vascular cell adhesion molecule-1." But of course the chemical formula for nitric oxide is NO and not N2O! HAHAHA you fools! To my knowledge nitrous oxide does not have the useful vasodilatory effects nitric oxide does in the treatment of ACS. While it might be useful in the same sense that heroin would be (anesthesia) you would be decreasing your FIO2 by displacing O2 with another gas. Then again, chugging a bottle of baby heroin would presumably decrease your respiratory drive so I guess you can feel free to pick your poison.

In light of this snap reconsideration, I will accept both B and C.



03.08.11
by

Intern Report Case 3.3


Case Presentation by Dr. Ryan Doss

A 28 year old male with a PMH of sickle cell disease presents to the emergency department complaining of a one day history of worsening shortness of breath and a subjective sensation of fever. He states this was preceded by 3 days of intractable "sickle cell crisis" pain unrelieved by his home pain medications. When questioned further about the nature of this pain, he reports lower back and bilateral lower extremity pain which is typical of his previous sickle cell crises. After thinking about it, however, he does report that this time a new right lower chest pain accompanied his usual symptoms. His home medications include morphine and dilaudid po.

Physical Exam:
Vitals: BP 128/62, HR 108, RR 30, Sat 93% on RA, and Temp 38.1C
General:He appears to be anxious and in mild respiratory distress with no accessory muscle use.
HEENT: NC/AT, PERRL, mucous membranes moist
CV: S1 S2 present, regular rhythm and tachycardic rate, no murmurs
Resp: Tachypnea, equal rise and fall, rales auscultated in the RLL
Abd: Soft, nondistended, nontender all 4 Qs
Ext: Peripheral pulses present in all 4 limbs, cap refill <2 seconds, strength 5/5 proximally and distally in all 4 limbs
Back: No tenderness to palpation throughout cervical, thoracic, and lumbar spine. No bony deformity, crepitus, or step-offs noted.
Neuro: A&Ox3, alert, cooperative, no gross focal deficits

An AP and lateral chest radiograph is obtained with the following results:


An ABG is obtained on room air:
7.48/31/81/23/92

Laboratory abnormalities include:
Hb 8.4, WBC 13,000

Questions:

1.  Calculate this patient's A-a gradient assuming an FiO2 of 21% (room air) and an Atm pressure of 760 (sea level.)
a) 10
b) 30
c) 5
d) 20
e) 40

2.  Of the following, which is the most common complication of acute chest syndrome?
a) Arrythmia
b) Mesenteric ischemia
c) Seizures
d) Acute kidney injury
e) Myocardial infarction

3.  Which of the following pathogens is most likely associated with acute chest syndrome?
a) Chlamydia pneumoniae
b) Legionella
c) Streptococcus pneumoniae
d) Staph aureus
e) Neisseria meningitidis

4.  Imagine you're lost in the woods, have sickle cell, get dehydrated, and develop an acute chest syndrome. Which of the following devices would you most wish you had brought? Also, it's 1910.
a) Horace P. Winterbottom's Patented Roentogram Generator
b) A tank of phlogisticated laughing anesthetic
c) Bayer Pharmaceutical's "Mother's Relief" Infant Teething Aide with Heroin
d) "Poseidon's Bane" Drowning Resuscitation Tobacco Smoke Enema Kit
e) A hearty sample of mandrake root and a crossroads in which to bury it, post-haste

Please submit your answers as a comment. Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving's: Intern Report.


03.08.11
by

Intern Report Case 3.3


Case Presentation by Dr. Ryan Doss

A 28 year old male with a PMH of sickle cell disease presents to the emergency department complaining of a one day history of worsening shortness of breath and a subjective sensation of fever. He states this was preceded by 3 days of intractable "sickle cell crisis" pain unrelieved by his home pain medications. When questioned further about the nature of this pain, he reports lower back and bilateral lower extremity pain which is typical of his previous sickle cell crises. After thinking about it, however, he does report that this time a new right lower chest pain accompanied his usual symptoms. His home medications include morphine and dilaudid po.

Physical Exam:
Vitals: BP 128/62, HR 108, RR 30, Sat 93% on RA, and Temp 38.1C
General:He appears to be anxious and in mild respiratory distress with no accessory muscle use.
HEENT: NC/AT, PERRL, mucous membranes moist
CV: S1 S2 present, regular rhythm and tachycardic rate, no murmurs
Resp: Tachypnea, equal rise and fall, rales auscultated in the RLL
Abd: Soft, nondistended, nontender all 4 Qs
Ext: Peripheral pulses present in all 4 limbs, cap refill <2 seconds, strength 5/5 proximally and distally in all 4 limbs
Back: No tenderness to palpation throughout cervical, thoracic, and lumbar spine. No bony deformity, crepitus, or step-offs noted.
Neuro: A&Ox3, alert, cooperative, no gross focal deficits

An AP and lateral chest radiograph is obtained with the following results:


An ABG is obtained on room air:
7.48/31/81/23/92

Laboratory abnormalities include:
Hb 8.4, WBC 13,000

Questions:

1.  Calculate this patient's A-a gradient assuming an FiO2 of 21% (room air) and an Atm pressure of 760 (sea level.)
a) 10
b) 30
c) 5
d) 20
e) 40

2.  Of the following, which is the most common complication of acute chest syndrome?
a) Arrythmia
b) Mesenteric ischemia
c) Seizures
d) Acute kidney injury
e) Myocardial infarction

3.  Which of the following pathogens is most likely associated with acute chest syndrome?
a) Chlamydia pneumoniae
b) Legionella
c) Streptococcus pneumoniae
d) Staph aureus
e) Neisseria meningitidis

4.  Imagine you're lost in the woods, have sickle cell, get dehydrated, and develop an acute chest syndrome. Which of the following devices would you most wish you had brought? Also, it's 1910.
a) Horace P. Winterbottom's Patented Roentogram Generator
b) A tank of phlogisticated laughing anesthetic
c) Bayer Pharmaceutical's "Mother's Relief" Infant Teething Aide with Heroin
d) "Poseidon's Bane" Drowning Resuscitation Tobacco Smoke Enema Kit
e) A hearty sample of mandrake root and a crossroads in which to bury it, post-haste

Please submit your answers as a comment. Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving's: Intern Report.


03.04.11
by

Intern Report Case Discussion 3.2

Case Presentation by Dr. Jeanise Butterfield



Discussion:
This patient is in adrenal crisis which is likely precipitated by abrupt steroid withdrawal following a long hospitalization for acute COPD exacerbation and pneumonia.  Recognition of adrenal crisis and prompt administration of hydrocortisone is critical to patient survival.  Adrenal crisis may result from an acute exacerbation of chronic adrenal insufficiency, adrenal hemorrhage, or abrupt withdrawal of steroids in patients with adrenal atrophy.  It usually occurs in response to major stressors such as sepsis, myocardial infarction, surgery, major injury or trauma. 

The predominant clinical manifestation of adrenal crisis is shock.  Symptoms include weakness, abdominal pain, anorexia, confusion, and fever.  Patients may be hypotensive and hypoglycemic but other physical findings in patients with adrenal insufficiency may be subtle and nonspecific.  Laboratory evaluation may reveal hyponatremia, hyperkalemia, and hypercalcemia. 

Glucocorticoids are essential to the management of adrenal crisis and should be administered immediately upon clinical suspicion.  The preferred glucocorticoid is hydrocortisone 100 mg IV.  Dexamethasone 6-8 mg IV can also be used and has the advantage of not interfering with ACTH stimulation test. 

As always, treatment begins with maintenance of airway, breathing and circulation.  Should a patient require intubation, etomidate should be avoided as an agent for RSI because it is a steroid synthesis inhibitor and may worsen hemodynamics in shock patients.   Aggressive fluid replacement may be required as well as correction of electrolyte abnormalities including hypoglycemia, hyponatremia, hyperkalemia and hypercalcemia.  Fluid replacement should be initiated with 0.9% normal saline, but may be changed to D5NS.  D50 may be required depending on the extent of hypoglycemia. 

It is important to uncover and treat the underlying problem that precipitated the crisis.  

Answers

1. D.  In the setting of adrenal crisis, glucocorticoids, preferably hydrocortisone 100 mg IV, should be administered immediately.  Do not await results of ACTH stimulation testing. CT scan and surgical consult may be indicated after steroid replacement to help diagnose or treat the precipating cause. 

2. C.  Patients in adrenal crisis may present with several electrolyte abnormalities including hyponatremia, hyperkalemia and hypercalcemia.  An early EKG manifestation of hyperkalemia is peaked t waves.  U waves are present in hypokalemia.  

3. E.  Ketoconazole and etomidate impair adrenal hormone synthesis.  Phenytoin and rifampin increase steroid metabolism. 


Pearls:
Think of adrenal crisis in the setting of hypotension refractory to volume resuscitation and catecholamines.

Patients with history of primary adrenal insufficiency (eg Addison's Disease) will require increased doses of steroids in the event of increased stress or illness. 

The most common iatrogenic cause of adrenal crisis is rapid withdrawal of steroids in the patients with adrenal atrophy secondary to long term steroid administration.

If you suspect adrenal crisis, immediately administer glucocorticoids.  Do not wait for ACTH stimulation test or serum cortisol.  


03.04.11
by

Intern Report Case Discussion 3.2

Case Presentation by Dr. Jeanise Butterfield



Discussion:
This patient is in adrenal crisis which is likely precipitated by abrupt steroid withdrawal following a long hospitalization for acute COPD exacerbation and pneumonia.  Recognition of adrenal crisis and prompt administration of hydrocortisone is critical to patient survival.  Adrenal crisis may result from an acute exacerbation of chronic adrenal insufficiency, adrenal hemorrhage, or abrupt withdrawal of steroids in patients with adrenal atrophy.  It usually occurs in response to major stressors such as sepsis, myocardial infarction, surgery, major injury or trauma. 

The predominant clinical manifestation of adrenal crisis is shock.  Symptoms include weakness, abdominal pain, anorexia, confusion, and fever.  Patients may be hypotensive and hypoglycemic but other physical findings in patients with adrenal insufficiency may be subtle and nonspecific.  Laboratory evaluation may reveal hyponatremia, hyperkalemia, and hypercalcemia. 

Glucocorticoids are essential to the management of adrenal crisis and should be administered immediately upon clinical suspicion.  The preferred glucocorticoid is hydrocortisone 100 mg IV.  Dexamethasone 6-8 mg IV can also be used and has the advantage of not interfering with ACTH stimulation test. 

As always, treatment begins with maintenance of airway, breathing and circulation.  Should a patient require intubation, etomidate should be avoided as an agent for RSI because it is a steroid synthesis inhibitor and may worsen hemodynamics in shock patients.   Aggressive fluid replacement may be required as well as correction of electrolyte abnormalities including hypoglycemia, hyponatremia, hyperkalemia and hypercalcemia.  Fluid replacement should be initiated with 0.9% normal saline, but may be changed to D5NS.  D50 may be required depending on the extent of hypoglycemia. 

It is important to uncover and treat the underlying problem that precipitated the crisis.  

Answers

1. D.  In the setting of adrenal crisis, glucocorticoids, preferably hydrocortisone 100 mg IV, should be administered immediately.  Do not await results of ACTH stimulation testing. CT scan and surgical consult may be indicated after steroid replacement to help diagnose or treat the precipating cause. 

2. C.  Patients in adrenal crisis may present with several electrolyte abnormalities including hyponatremia, hyperkalemia and hypercalcemia.  An early EKG manifestation of hyperkalemia is peaked t waves.  U waves are present in hypokalemia.  

3. E.  Ketoconazole and etomidate impair adrenal hormone synthesis.  Phenytoin and rifampin increase steroid metabolism. 


Pearls:
Think of adrenal crisis in the setting of hypotension refractory to volume resuscitation and catecholamines.

Patients with history of primary adrenal insufficiency (eg Addison's Disease) will require increased doses of steroids in the event of increased stress or illness. 

The most common iatrogenic cause of adrenal crisis is rapid withdrawal of steroids in the patients with adrenal atrophy secondary to long term steroid administration.

If you suspect adrenal crisis, immediately administer glucocorticoids.  Do not wait for ACTH stimulation test or serum cortisol.  


02.27.11
by

Intern Report Case 3.2

Case Presentation by Dr. Jeanise Butterfield

A 58-year-old woman presents to the emergency department with severe abdominal pain, generalized weakness and subjective fever.    She is able to tell you that the pain began yesterday and has been gradually getting worse since onset but she is so weak that she only speaks in short phrases.  The pain is constant and cramping in nature, getting worse.  She has had 2-3 episodes of emesis per day and decreased appetite.   She has been feeling very warm but has not taken her temperature.   No diarrhea, last BM yesterday. 

She has a history of COPD and hypertension and was recently discharged from an outside hospital after a lengthy stay for COPD exacerbation and pneumonia which required intubation.  She was given several prescriptions to fill including inhalers and pills but could not secondary to lack of insurance and financial issues.   

PMH: COPD, HTN but noncompliant with medications
Meds:  None
Allergies: NKDA
FH: Hypertension
SH: Occasional alcohol use.  25 pack year tobacco history but quit 5 years prior. Denied illicit drug use.


PE:     Vital Signs - BP 96/64, heart rate 108, respiratory rate 24, temp 38.2°C, pulse ox 96% on RA
           HEENT: Atraumatic, normocephalic; PERRL, EOMI; dry mucus membranes                 
General - Thin female lying still in fetal position on stretcher
Skin - Diaphoretic, pale, no rashes
           Cardiovascular - Tachycardic, regular rhythm, no murmurs
Respiratory - Tachypneic, decreased breath sounds at the right base, slight expiratory wheeze bilaterally, no accessory muscle use
Abdominal - Soft, nondistended, diffusely tender to palpation, + guarding, no rebound, normal bowel sounds,
            Musculoskeletal - Full ROM in all 4 extremities, no edema, symmetric pulses bilateral UE & LE
Neuro - A&O x 3, normal speech and hearing, face is symmetric, sensation equal and intact throughout, motor is decreased in all extremities but symmetric, patient not exerting much effort                 
                 
Pertinent Labs:
                  Sodium 128 mEq/L, potassium 5.8 mEq/L, glucose 55 mg/dL, cortisol 20 µg/dL. 

Questions

1.  Immediate management of the patient should include:
                  a. Surgical consultation
                  b. Abdominal CT
                  c. Morphine
                  d. Hydrocortisone
                  e. ACTH stimulation test

2. If an EKG was performed on this patient, which abnormality could be expected
                  a. ST elevation
                  b. Right bundle branch block
                  c. Peaked T waves
                  d. Prolonged QT interval
                  e. Prominent U waves

3. Which of the following is least likely to precipitate acute adrenal insufficiency:
                  a. Etomidate
                  b. Phenytoin
                  c. Ketoconazole
                  d. Rifampin
                  e. Nitroglycerine

Please submit your answers as a comment. Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving's: Intern Report.


02.27.11
by

Intern Report Case 3.2

Case Presentation by Dr. Jeanise Butterfield

A 58-year-old woman presents to the emergency department with severe abdominal pain, generalized weakness and subjective fever.    She is able to tell you that the pain began yesterday and has been gradually getting worse since onset but she is so weak that she only speaks in short phrases.  The pain is constant and cramping in nature, getting worse.  She has had 2-3 episodes of emesis per day and decreased appetite.   She has been feeling very warm but has not taken her temperature.   No diarrhea, last BM yesterday. 

She has a history of COPD and hypertension and was recently discharged from an outside hospital after a lengthy stay for COPD exacerbation and pneumonia which required intubation.  She was given several prescriptions to fill including inhalers and pills but could not secondary to lack of insurance and financial issues.   

PMH: COPD, HTN but noncompliant with medications
Meds:  None
Allergies: NKDA
FH: Hypertension
SH: Occasional alcohol use.  25 pack year tobacco history but quit 5 years prior. Denied illicit drug use.


PE:     Vital Signs - BP 96/64, heart rate 108, respiratory rate 24, temp 38.2°C, pulse ox 96% on RA
           HEENT: Atraumatic, normocephalic; PERRL, EOMI; dry mucus membranes                 
General - Thin female lying still in fetal position on stretcher
Skin - Diaphoretic, pale, no rashes
           Cardiovascular - Tachycardic, regular rhythm, no murmurs
Respiratory - Tachypneic, decreased breath sounds at the right base, slight expiratory wheeze bilaterally, no accessory muscle use
Abdominal - Soft, nondistended, diffusely tender to palpation, + guarding, no rebound, normal bowel sounds,
            Musculoskeletal - Full ROM in all 4 extremities, no edema, symmetric pulses bilateral UE & LE
Neuro - A&O x 3, normal speech and hearing, face is symmetric, sensation equal and intact throughout, motor is decreased in all extremities but symmetric, patient not exerting much effort                 
                 
Pertinent Labs:
                  Sodium 128 mEq/L, potassium 5.8 mEq/L, glucose 55 mg/dL, cortisol 20 µg/dL. 

Questions

1.  Immediate management of the patient should include:
                  a. Surgical consultation
                  b. Abdominal CT
                  c. Morphine
                  d. Hydrocortisone
                  e. ACTH stimulation test

2. If an EKG was performed on this patient, which abnormality could be expected
                  a. ST elevation
                  b. Right bundle branch block
                  c. Peaked T waves
                  d. Prolonged QT interval
                  e. Prominent U waves

3. Which of the following is least likely to precipitate acute adrenal insufficiency:
                  a. Etomidate
                  b. Phenytoin
                  c. Ketoconazole
                  d. Rifampin
                  e. Nitroglycerine

Please submit your answers as a comment. Your submission will not immediately post.  Answers with a case discussion will post on Friday.  If you have any difficulty, please contact the site administrator at arosh@med.wayne.edu. Thank you for participating in Receiving's: Intern Report.