UMEM Educational Pearls

Can You Rely on Your Clinical Impression to Exclude SBP?

• SBP is an important can't miss diagnosis, as the mortality rate even for treated patients is approximately 20%
• The incidence of SBP ranges from 2.5% (clinic setting) to 12% of all patients admitted with decompensated cirrhosis
• SBP is diagnosed by a neutrophil count > 250 or a positive ascitic fluid culture obtained via paracentesis

• Can our clinical impression exclude SBP without performing a paracentesis? Unfortunately, the answer is NO.
• Sensitivity of physician clinical impression is just about 75%, with a specificity of 34%
• Fever is uncommon in patients with SBP (sensitivity as low as 17%)
• Take Home Point: only a diagnostic paracentesis can reliably exclude SBP in patients admitted for decompensated cirrhosis

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Cerebral Venous Sinus Thrombosis (CVST)

An uncommon but very serious entity that leads to three distinct types of presentations:

• Headache
• Seizures
• Stroke

Caused by thrombosis of one of the intracerebral venous sinuses (most commonly the transverse sinus) The major risk factor is hypercoagulable disease. May be the underlying cause of a majority of cases of idiopathic intracranial hypertension.

When to suspect:

• Headache with negative CT, negative LP, but high opening pressure
• In any patient with new onset idiopathic intracranial hypertension (i.e. pseudotumor cerebri). Can't be formally diagnosed without a negative MRI.
• Stroke syndrome that doesn't quite fit. May see bilateral infarcts in the posterior regions. These are actually venous infarcts secondary to the sinus thrombosis.

Diagnosis:

• Just like a lot of other things in medicine, "If you don't think about it, you can't diagnose it."
• 1 in 3 head CT scans will be normal
• MRI with MRV (venous phase) is the diagnostic standard

Treat:

• Anticoagulation with heparin then warfarin

An estimated 20-30% of patients with ACS end up having no identifiable culprit lesion on angiography. Almost half of these patients have inducible coronary spasm. Although these patients have a good outcome, they also have a tendency to return to the hospital for frequent re-evaluations. Evaluation for and treatment of spasm can improve the quality of life for these patients and also to decrease re-visits.

When patients with reports of "clean" coronaries return to the ED with a concerning presentation for ACS, one of the considerations should be coronary spasm. Consider prompting the primary care physician or admitting team to look into this possibility, as it may result in a reduction in recurrent ED visits.

Severe Hypothyroidism or Myxedema Coma

• Mortality rate has been as high as 80% now 15-20% with aggressive treatment
• Some common symptoms are:
  • Constipation
  • Depression
  • Lethargy
  • Dry, Brittle hair or Alopecia
  • Weight Gain
  • Cold Intolerance
  • Weight Gain
• Treatment consists of:
  • Rule out aggravating cause (i.e.: infection)
  • Start IV levothyroxine dosing
    • Initial dose 400-500 mcg (Helps to saturate the thyroid receptors)
    • Daily dose 100 mcg/day
  • Consider starting Dexamethasone or doing a Cortisol stimulation test
    • Patients may also have adrenal insufficiency from primary pituitary failure or may have secondary adrenal suppression due to the severe hypothyroidism.  If dexamethasone is not provided they may develop severe adrenal insufficiency once you kick start their metabolism.

Pediatric Discitis is an intervertebral disc infection due to hematogenous spread to vascular channels in cartilage that disappear later in life.  In 1/3 of patients it is caused by S. aureus.

Presenting Features

• age <2.5 years (75%) 
• Refuse or difficult to walk  (56%)
• Back/neck pain (25-45%) ( 100%>3years)
• Hx of fever (28-47%)
• lumbaosacral area (78-82%)
• Mean ESR 39-42
• WBC> 10,500 (50%)
• Abnormal MRI 90-100 %

Management is to exclude more severe disease (osteomylelitis,abscess, tumor) and antibiotic use is debatable.  Remember children this age rarely complain of back pain. 

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Clinical Manifestations in relation to lead level in children:

• > 70 - 100 mcg/dL: Encephalopathy, increased ICP, anemia, vomiting
• 50 - 70 mcg/dL: Irritable, difficult child, abdominal pain, anorexia
• >10 mcg/dL: often asymptomatic, may develop impaired cognition, behavior, impaired fine-motor coordination, hearing and growth

Tension gastrothorax?

• Tension gastrothorax is a life threatening condition characterized by herniation of the stomach through a defect in the diaphragm with compression of the mediastinal contents
• Although many cases occur in pediatric patients (secondary to congenital defects), adults with a history of diaphragmatic injury are at risk (also patients with a type III or IV hiatal hernia)
• The clinical presentation is the same as a tension pneumothorax - hypotension, tachycardia, hypoxia, JVD, and decreased breath sounds
• CXR appearance can be very similar to tension pneumothorax, however, the treatment is substantially different
• Needle decompression and tube thoracostomy are contraindicated, as this may cause visceral perforation
• The treatment of choice is NGT (or OGT) decompression followed by surgical repair

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 Does Hypertension (elevated BP) Cause Headache?

This is an age old question that many of us have struggled with in the ED for many years...

Other questions include: Does elevated BP cause headaches? Do we need to scan hypertensive patients with headache just because they have a headache? At what level of BP does the BP actually cause headache? 

A few quick pearls:

• Although incredibly high BPs (diastolics above 130 mm Hg) have been correlated with headache, the general concensus is that hypertension doesn't really cause headaches. 
• At really high blood pressures (again, diastolic BP > 130-140), cerebral autoregulation breaks down and may lead to cerebral edema and headache...hypertensive encephalopathy.
• Elevated systolic BP may actually be protective for developing headaches
• CT scanning the hypertensive patient with a headache is not warranted a lot of the time, unless the patient has a neuro deficit, or if the headache was acute onset or associated with other findings of hypertensive encephalopathy.
• Patients with HTN are as likely to have a headache in the ED as non-hypertensive patients

Severe emotional stress is well-reported to produce an unusual transient cardiomyopathy that mimics cardiac ischemia or infarction on ECG as well as biomarker testing. On angiography, the coronaries are often clean. The ventriculogram takes on an apical or mid-ventricular ballooning appearance due to akinesis. In the ED, these patients will look just like a real thrombosis-related case of ACS and they often develop cardiogenic shock. Unlike true AMI-related cardiogenic shock, these patients have an excellent prognosis...if treated aggressively early-on with supportive therapy (e.g. pressors).

Intracranial catastrophes, such as hemorrhage, ischemic stroke, and head trauma; and severe medical illnesses, such as sepsis, pheochromocytoma, and catecholamine-excess states, are also reported to produce a similar syndrome of LV dysfunction.

The takeaway points: (1) severe emotional stress can be deadly...be wary of diagnosing "anxiety" or "panic attack" without checking an ECG; (2) check an ECG early in the course of any patients with the above conditions that look sick; (3) if the ECG shows signs of severe ischemia, aggressive treatment can be life-saving.

[ref: Bybee KA, Prasad A. Stress-related cardiomyopathy syndromes. Circulation 2008;118;397-409.]

Mallet Finger:

A common injury resulting in a tear or avulsion of the extensor digitorium tendon inserting into  the base of the distal phalanx.  Occurs due to hyperflexion of the finger usually as of a esult of it getting jammed on a ball while playing sports.  Most can be treated non-surgically.

The distal phalanx must be kept in full extension for 6 to 8 weeks. This is one of the few times that the finger should not be splinted in the position of function.

Make sure that patient is informed that if they remove the splint and flex their finger the 6 to 8 week healing window will be reset to day 0.  These patients should not be doing ROM exercises and must wear the splint full time.

Popsicle or cold panniculitis is an inflammation of the subcutaneous fat after prolonged exposure to cold.  It is thought to occur more often in infants and young children because they have a higher percentage of saturated fatty acids than older children and adults.  Pediatric patients may present to you to be evaluated/ruled out for abuse by social workers, schools, or police and if you have the correct history it is easy to dispo quickly.

Clinical Features of Popsicle Panniculitis

• Absence of systemic signs
• Minimal pain, with or without
• Skin is red to purplish, indurated, may have discrete nodules or plaques
• perioral location for popsicles, but may occur at any other area of skin exposure
• resolves in 2-3 weeks without scarring
• hyperpigmentation may persist
• arises within hours to to 1-2 days after exposure to a cold object

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Several antihypertensive agents raise intracranial pressure. Normal cerebral blood flow (CBF) is constant within normal cerebral perfusion pressure (CPP) ranges, recalling that CPP=MAP-ICP.

If CPP is outside the range in which autoregulation occurs, e.g. due to a structural lesion, ischemic stroke, or head trauma, CBF decreases and can adversely affect the patient.

• Nitroprusside
  • Vasodilates both cerebral arteries and veins, increasing ICP
  • Inhibits the normal vasoconstrictive response to hypocapnia
• Nitroglycerin
  • Causes cerebral venodilation, increasing ICP
  • Impairs vasodilatory response to hypercapnia
• Hydralazine (varying effects)
  • Vasodilates cerebral arteries > cerebral veins
  • Impairs cerebral autoregulation
• Nicardipine
  • Other calcium channel blockers increase ICP by vasodilating arteries
  • Has been used to treat vasospasm in SAH
  • Increases cerebral blood flow in patients with SAH and acute stroke

In patients with ischemic stroke or intracerebral pathology, labetalol or esmolol may be used to lower blood pressure without raising ICP. Nicardipine is recommended for use in patients with ischemic stroke or SAH but not in patients with brain injury

If the patient has NO structural abnormalities, but has hypertensive encephalopathy, nitroglycerin, nitroprusside, labetalol, esmolol, or nicardipine may be used.

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• Encephalomalacia, also known as cerebromalacia, is a softening of brain tissue that results from ischemia or inflammation, most typically due to vascular insufficiency or degenerative changes.

• On Brain CT, it appears as a darkened area and can be confused for cerebral edema due to acute ischemia (i.e stroke).

• Unlike edema, encephalomalacia on CT is often accompanied by:

                    ---  well defined, circular vacuoles

                    ---  presence of good gray-white matter differentiation in surrounding areas

                    ---  a lack of significant effacement or lost of sulcus definition

                    ---  a history of prior stroke or head injury

Subcutaneous Insulin in the Critically Ill

• Although intensive insulin therapy in the critically ill remains controversial and a matter of much debate, hyperglycemia is common in the critically ill ED patient
• Hyperglycemia is associated with worse outcomes in this patient population
• When treating hyperglycemia in the critically ill ED patient, use caution with subcutaneous insulin
• Absoprtion of insulin administered subcutaneously is slow, erratic, and highly variable often due to poor perfusion, hypotension, and/or vasopressor therapy
• In these patients, IV insulin is a better route of administration and leads to more reliable control of hyperglycemia
• Recall that the onset of action of insulin given IV is 10 - 30 minutes, with a duration of action of about 1 hour

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Avoidable Pitfalls in Managing the Hypertensive Patient

We all see very hypertensive patients on almost every shift. Dr. Winters has an earlier pearl related to pitfalls in treating patients with hypertensive encephalopathy, but I thought it was time to reiterate just a few points.

• No evidence to date has ever shown a benefit to acutely lowering someone's BP in the ED prior to discharge
• Probably the best thing you can do for the patient with out of control BP is to arrange (and make sure they have) followup for the next day or two after discharge
• In patients with severe HTN (eg. admitted patients with pressure to high to go to their inpatient bed), avoid agents like IV Hydralazine. This agent is pretty reliable in being completely unpredictable when it comes to BP response. Some will really bottom out their BPs.
• Avoid Clonidine unless the patient is on it and stopped taking it recently (rebound HTN). May worsen someone's already crappy mental status.
• If a patient is being admitted, say to a unit or step down unit, don't bother titrating oral agents for people with pressures > 240/130 mm Hg or so. Consider a drip-oral agents may "stack" and take effect, thus lowering someones BP way lower than you wanted.
• Don't treat the number, treat the patient.

 A normal ECG should not be a huge source of relief when evaluating patients with possible or confirmed myocardial infarction. 8% of acute myocardial infarctions have a completely normal ECG at the time of presentation, and these patients have a 5.7% in-hospital mortality. Serial electrocardiography can certainly improve the yield of electrocardiography but does not rule out AMI with 100% accuracy.

Like most tests in medicine, the ECG is very useful at ruling in disease, but it is limited at ruling out disease.

[The Prognostic Value of a Normal or Non-specific Initial ECG in AMI. JAMA 2001.]
 

Paracentesis Part II- Ascites Fluid Analysis:

See last weeks procedure pearl for some hints on doing a paracentesis..

Now that you have the fluid what should you send it for:

• Cell Count
• Gram Stain and Culture
• Amylase (normal value is half serum)
• Albumin
• Consider cytology if  cancer is a consideration

Now for the analysis:

• WBC Count >250 PMNs generally accepted as consistent with infection.  Especially if there is more than 70% PMNs which is the upper limit of normal. SAAG (Serum - Ascites Albumin Gradient) an easy calculation to differentiate what the cause of the ascites might be from:
  • Subtract the patient's ascites albumin from the serum albumin (Serum Albumin - Ascites Albumin = SAAG)
  • SAAG > 1.1 mg/dL(Due to items that increase portal pressures)
    • Cirrhosis
    • Alcoholic Hepatitis
    • Cardiac Ascites
    • Hepatic Failure
    • Budd-Chiari Syndrome
    • Portal Vein Thrombosis
    • Myexdema
    • Others
  • SAAG < 1.1 mg/dl (due to intraabdominal forces causing increased oncotic pressure)
    • Tuberculosis Peritonitis
    • Pancreatitic Ascites (typically while have elevated amylase in ascitic fluid)
    • Bowel Obstruction
    • Nephrotic Syndrome
    • Biliary Ascites
    • others

** Corrected definition of SAAG as it was initially reversed.  Thanks to Dr. McCurdy on his proof reading.

 Melamine

• In case you thought the chinese only sent their toxin filled products to the USA, a massive scandal has been occurring with their milk.
• Adding melamine to their milk, companies were able to get falsely elevated readings of protein which is measured by the government to make sure the milk was not watered down.
• 53,000 illnesses, over 12,000 hospitilizations and at least 4 infant deaths have been attributed to their milk supply - 20% of China's milk supply is thought to be contaminated
• Melamine or melamine resin is used to make plastics and involved in other polymeric reactions.
• Toxicity involves the creation of kidney stones - imagine the pain in these poor children
• These children died from renal failure from multiple kidney stones.
• Check the link below to the news article

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• Acceleration, deceleration, and rotational forces cause diffuse axonal injury (DAI).
• It is characterized by widespread shearing and retraction of axons during traumatic brain injury (TBI).
• DAI often results in coma and is associated with poor prognosis.
• In addition to cortical white matter injury, it often also involves the corpus callosum, basal ganglia, brainstem, and cerebellum.
   

AIDS: coming to a critically ill patient in your ED

• Acute intestinal distress syndrome (AIDS) is a recently coined term used in the continuum of intraabdominal hypertension (IAH) to abdominal compartment syndrome (ACS)
• In previous pearls we have discussed the importance of IAH in the critically ill and how to measure intraabdominal pressure (IAP)
• Recall that IAH is defined as a sustained elevation of IAP > 12 mmHg
• The focus of attention is shifting to "secondary ACS" - it is highly prevalent in the critically ill and is independently associated with increased mortality
• Sepsis is a cause of secondary ACS and is the most likely condition we will encounter in our critically ill patient population
• Current recommendations suggest that IAP be measured daily in patients at risk for IAH (i.e. the septic ED patient)

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