Hypertensive Encephalopathy (HE) is a clinical diagnosis and can look like many other disease entities.
HE refers to a relatively rapidly evolving syndrome of severe hypertension in association with severe headache, nausea, and vomiting, visual disturbances, convulsions, altered mental status and, in advanced cases, stupor and coma.
The key is the presence of severe hypertension. Remember, though, that 160/105 mm Hg may be high for an individual patient. Most patients with the syndrome will have diastolic pressures well in excess of 120-130 mm Hg. The only way you will know if the diagnosis is correct is to treat the BP (carefully control), work up other etiologies, and see of symptoms improve with BP control.
Beware the patient with severe HTN and seizure. Seizure may be the first, and only, symptom of hypertensive encephalopathy.
Some confusion exists regarding proper distinction and treatment between the different tachydysrhythmias associated with WPW. Here's the scoop:
1. orthodromic SVT: narrow regular tachycardia, looks just like a routine SVT, treat just like any other SVT (AV nodal blockers work fine)
2. antidromic SVT: wide regular tachycardia, looks just like VTach, treat like VTach (amiodarone, procainamide, shock; lidocaine won't work, though won't harm either)
3. atrial fibrillation: very different!! irregularly irregular, morphologies of the QRS complexes vary between narrow and wide, some areas may have rates as high as 250-300/min, MUST avoid all AV nodal blockers (which includes adenosine, CCBs, BBs, digoxin, amiodarone); treat with procainamide or sedation+cardioversion
Adhesive Capsulitis -- Frozen Shoulder
In a previous pearl we were discussing the need to perform EGD for any suicidal patient with a history of ingestion of a caustic to grade injury and assess chance of perforation and/or stricture formation. Suicidal patients are intentionally ingesting the caustic and can thus justify the risk/benefit ratio more easily than the pediatric unintentional ingestion. The concerned parent will bring the child in with a possible ingestion of a caustic. The container could be simply in the same room, spilled on the child and never be ingested. Even if ingested, the amount is less if the child tastes the caustic and will reflexively cause spitting. The literature is scant in regards to this type of patient but seems to point to this general algorithm:
Child displays 2 or more of the following symptoms there is enough evidence from case series that there will be a clinically signficant lesion found on EGD.
Vomiting, Drooling, Stridor, Presence of Oropharyngeal Burns
That being said, many clinicians would elect for EGD and assessment of airway with stridor alone. Do not be fooled into thinking if you see no oral lesions that there is no way the child ingested the caustic. Each case series showed a lack of correlation of physical exam findings to EGD findings.
-- ulnar nerve >>> supplies palmar surface and dorsal tips of little finger and medial half of ring finger, including
adjacent parts of hand.
-- median nerve >>> supplies palmar and dorsal aspects of thumb, index finger, middle finger, and lateral half
of ring finger, including adjacent parts of hand.
-- radial nerve >>> supplies most of dorsal surface of hand.
Hemostatic Therapy for ICH - Updated Guidelines
Beta Blockade in Treating Acute Aortic Dissection
Medical therapy for acute aortic dissection is aimed at decreasing shear stress within the aorta. Although there are many agents to choose from when treating hypertension in patients with acute aortic disease, all regimens should include a beta blocker (like esmolol) unless contraindicated. Initiation of a beta blocker before another antihypertensive agent is added is crucial as this will prevent reflex tachycardia associated with vasodilators and other afterload reducers. Reflex tachycardia may worsen the dissection.
typical ECG findings associated with hypercalcemia: short QT (e.g. QTc < 400 msec), ST-segment depression
typical ECG findings associated with hypocalcemia: prolonged QT
note that hyperkalemia is often associated with hypocalcemia, and as a result hyperkalemic patients often have a prolonged QT, but it's not the hyperkalemia that prolongs the QT, it's the hypocalcemia
Rotator Cuff Tears:
Four muscles make up the rotator cuff (SITS) which control internal and external rotation of the shoulder and abduct the shoulder.
Tears can be due to acute injuries (falls, heavy lifting, forceful abduction), though the majority (>90%) of rotator cuff tears are chronic in nature and due to subacromial impingement and decreased blood supply to the tendons.
Most patients can be treated with sling immobilization, NSAIDs and referral to sports medicine or orthopaedic surgeons. Elderly patients should be referred quickly as prolonged immobilization can lead to a frozen shoulder.
We will all get the patient presenting with low blood glucose on a regular basis. In general, barring any underlying infection, those who are insulin dependent can be corrected with IV dextrose and/or food and be discharged. Those on a sulfonylurea may experience repeated hypoglycemic episodes and require admission - perhaps even treatment with the antidote: octreotide.
Below is the duration of action and half-life of the sulfonylureas which illustrates the need for admission:
Duration of action is the physiologic effect whereas the half-life is the pharmacokinetics of elimination of the drug. Often these two numbers are different for drugs. Do not let the half-life fool you into thinking it is safe to discharge a hypoglycemic patient on a sulfonylurea.
2. Distinguish artery from vein with compression and/or Doppler.*
3. Sterilely prep the site and ultrasound probe.
4. Cannulate the vein in the transverse or longitudinal plane.
Treatment of Cerebral Venous and Sinus Thrombosis
Thrombosis of the cerebral venous system, also known as cerebral venous and sinus thrombosis and dural sinus thrombosis, is an uncommon condition encountered in the emergency department. The diagnosis may be stumbled upon by various CT findings or by MRI and/or a high opening pressure on lumbar puncture.
The treatment of choice is full dose anticoagulation with heparin. Available studies looked at unfractionated heparin, but many experts now consider LMWH (like Lovenox) an acceptable alternative. Despite the risk of hemorrhagic transformation of a venous infarct, heparin therapy is considered the standard treatment for this condition.
Increasing literature is supportive of the idea of electrically cardioverting new-onset atrial fibrillation (onset < 48 hours). The traditional concerns are that (1) cardioversion doesn't work well with atrial fibrillation and that (2) you will induce an embolic event. The literature actually indicates that both of these concerns are not true. The success rate of electrically cardioverting new-onset atrial fibrillation is actually >90% and the risk of embolism is < 1% (Burton, Ann Emerg Med). Many EDs already utilize such protocols that recommend routine cardioversion for these patients and discharge after a brief observation period.
In coming years, fueled by issues pertaining to hospital overcrowding and cost containment, we'll all be seeing more and more papers and guidelines recommending early electrical cardioversion, so if you aren't comfortable with the idea....you will be!
Helpful clues in the evaluation of elbow trauma
Fat pads: The fat pad sign can be seen with any joint effusion (infection, inflammation) but in the setting of trauma, effusions are indicative of fractures about the elbow (even if no fracture line can be identified).
There are two fat pads within the elbow. Normally, on a true lateral radiograph only the anterior fat pad is seen as a small triangular radiolucent shadow anterior to the distal humeral diaphysis. The posterior fat pad is ordinarily not visualized on a lateral radiograph because it is tucked away within the olecranon fossa.
Normal lateral view: http://nypemergency.org/images/ElbowNormal.jpg
With fractures, the joint becomes distended with blood. The anterior fat pad becomes displaced superiorly and outward from the humerus giving the so called "sail sign." Similarly, the posterior fat pad gets displaced out of the olecranon fossa and becomes visible on the lateral radiograph.
Anterior (sail) and posterior fat signs: http://nypemergency.org/images/Elbowsfatpadarrow.jpg
A common debate on the topic of pediatric burns is whether or not blisters should be debrided. ALL PEDIATRIC BURN BLISTERS SHOULD BE DEBRIDED. There are two reasons for this:
1. Without debridement of burn blisters, the depth of a burn cannot be assessed, and such an assessment will certainly affect treatment and disposition.
2. There is conflicting (poor) evidence that blister fluid provides both protective and damaging properties, however, there is excellent evidence that ruptured blisters, or large blisters which are likely to rupture, carry a higher risk of infection if not debrided. Therefore, all blisters should be debrided.
The best method for debriding blisters uses sterile gauze soaked in saline, and it is important to note that pain is almost universally decreased after debridement.
The "1, 2, 3 Ouch!" technique is exactly what it sounds like (count to three with the child, and then wipe quickly, like tearing off a bandage), and works well in older children with smaller burn areas. Sedation may be necessary for extensive debridements, and these children may need to be taken to the OR for debridement under anesthesia. Some burn centers utilize non-operating room anesthesia (NORA) areas for such debridements that may be prolonged or painful, but do not require the full resources of an operating room.
If benzodiazepines and supportive care fail to improve agitation and correct vital signs, several case reports indicate the successful use of cyproheptadine, an antihistamine with nonspecific antagonist effects at 5-HT1A and 5-HT2A receptors.
Cyproheptadine is available in 4 mg tablets or 2 mg/5 mL syrup. When administered as an antidote for serotonin syndrome, an initial dose of 8-12 mg is recommended, followed by 2 mg every two hours until clinical response is seen. Cyproheptadine is only available in an oral form, but it may be crushed and given through a nasogastric tube.
Cyproheptadine may lead to sedation, but this effect is consistent with the goals of management. It may also produce transient hypotension due to the reversal of serotonin-mediated increases in vascular tone. Such hypotension usually responds to IV fluids. Cyproheptadine is rated category B for safety in pregnancy by the FDA.
Consider the diagnosis of a Cervicogenic Headache when the following findings are present:
A. Pain localized to the neck and occipital region, potentially with projection to forehead, orbits, temples, vertex or ears.
B. Pain is precipitated or aggravated by particular neck movements or sustained postures.
C . At least one of the following:
1. Resistance to or limitation of passive neck movements.
2. Changes in neck muscle contour, texture, tone or response to active and passive stretching and contraction.
3. Abnormal tenderness of neck muscles.
D. Radiological imaging reveals at least one of the following:
1. Movement abnormalities in flexion/extension.
2. Abnormal posture.
3. Fractures, congenital abnormalities, bone tumors, rheumatoid arthritis or other distinct pathology (not spondylosis or osteochondrosis).
Drug-Induced Hypophosphatemia
