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Archive for February, 2011|Monthly archive page

Abdominal pain

In EM2 on February 16, 2011 at 4:38 am

55yo M hx HTN presenting with one day of abdominal pain. diffuse, non-specific. states he’s felt constipated x1day. denies nausea or vomitting. tried to force a BM today, noted BRBPR. was seen in pmd office today, sent to ED for concern of abdominal bruit. no prior hx of AAA or abdominal surgeries.

PE: vital signs stable: BP 146/93, HR 106, RR 11, 93% on RA. Pt visibly uncomfortable, +Tenderness on deep palpation of lower abdomen bilaterally. heart/lungs otherwise within normal. +BRPPR(bright red blood per rectum). Bedside Ultrasound – AAA @9cm. ?rupture.

Outcome: STAT Vascular surgery consult. labs, CTabdomen/pelvis CT read: Infrarenal abdominal aortic aneurysm measuring up to 10.8 cm with stranding within the left adjacent anterior and posterior pararenal space concerning for rupture. hgb/hct 14.5/42.4; Creatinine = 0.4;  Patient went straight to the OR.  Patient remained awake and interactive throughout ED course (albeit emotional and tearful upon notification of his diagnosis).

Teaching point: diagnosis and acute management of AAA.

1.Clinical Suspicion (let your alarm bells ring!): Risk factors are males, hypertension, smoker, Artherosclerotic vascular disease, first degree relative with AAA, age>65. Regardless, it is imperative to maintain a high clinical suspicion for AAA even in the setting of normal vital signs. In patients >5oyo with acute abdominal/back/flank pain, the idea of a AAA should cross the EM physicians mind at least as part of the differential. Classic triad of pain, hypotension and abdominal mass is only present about 30% of the time. AAA rupture has about 80% mortality and any patient with large AAA should be considered unstable 2/2 potential to rapidly de-compensate.

Patients presenting with GI bleed complaints (melena or hematochezia) may have an aorto-enteric fisutla (may be primary – with an initial AAA or secondary after AAA repair). GI bleed is initially minor in the first few days but may progress to massive hemorrhage.

Patients presenting with high-output cardiac failure may have an aorto-venous fistula. This is when the AAA erodes into the IVC thus causing a shunt of blood into the IVC.

Patient may presenting with subacute back/flank pain that started sharp initially, subsided but is still persistent. There’s a concern of a low-grade retroperitoneal leak from the AAA. CT may show a chronic/organized hematoma which may be confirmed in the OR.

2. Imaging: BEDSIDE ULTRASOUND(US) is your friend! its quick, non-invasive and has a sensitivity/specificity approaching 100% for ruling in a AAA; shortens time to diagnosis and time to OR, can be done at bedside (great for the unstable patient that cant be transported to radiology). It may be limited by body habitus and excessive bowel gas. After age 50, the normal diameter of the infrarenal aorta is 1.5 cm in women and 1.7 cm in men. Aorta>3cm is considered AAA. an US can rule in/out a AAA. its harder to state if its ruptured based on US; A FAST exam can be done to evaluate for free fluid. AAA: <4cm – annual close monitoring with US; 4-5cm – q6mths US. >5cm – elective repair (20-40% risk of rupture).

CT scan: about 100% accuracy. will give better information about rupture, retroperitoneal bleed, or dissection.

3. Surgery consult: this should be done ASAP! before labs and before CT(if diagnosis is made on US). Patient is only ‘stable’ once they are in the OR with their aorta cross clamped!

4. Medical management: this is temporal until the patient can get definitive treatment in the OR. You know the drill: IV, O2, monitor, 2large bore IV’s. If patient is hypotensive, begin initial fluid resuscitation BUT what they really need is BLOOD. Get on the phone with blood bank, get that O(-) blood and start transfusing. Airway control as needed depending on patients’ mental status.

Post op complication: Graft infection, Aorto-enteric fistula, Pseudoaneurysm, Endoleak.

Refrences: Rosen’s 6th edition, chpt 85.

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Retained products.

In Uncategorized on February 13, 2011 at 10:44 pm

29yo F G4P3 LMP Nov 26th 2010 presenting with vaginal bleeding. The patient had a recent visit to the ED 2weeks ago with similar complaints, Pelvis US showed IUP at 7wks 4day without Fetal heart motion and concern for fetal demise (HCG@>13000). Patient was discharged home with close instructions to f/u with OB/GYN. She was seen at  a clinic where she was prescribed misoprostol 200mcg PO first and 300mcg PO 2days later; she took the medication but still noted lower abdominal cramping and vaginal bleeding over the past 3days that started heavy but was now slowing down.On exam, patient is afebrile and normotensive, HR @70 with mild bilateral lower abdominal/pelvic pain. Pelvic exam – cervical os is closed with minimal blood in the vault. no adenexa masses or tenderness.

WorkUp: repeat US – retained products of conception(RPOC) within the uterus. hcg<5000. Hbg was stable at 12. RH(+)

Teaching Point: Management of Retained Products of Conception

As with all things, the EM resident should have noted the following: Is the patient stable or unstable? Is the patient septic?

In an unstable or septic patient with RPOC, the management is surgical. A stat OB/GYN consult is necessary for prompt surgical evacuation of the uterus. In the mean time resuscitative efforts should have begun: IVF, Blood transfusion and broad spectrum antibiotics.

In a stable patient, the management may be expectant but is typically medical with Misoprostol (its safe, cheap, low side effect profile and usually the first choice by ob); its dosed 800mcg intravaginally x1 and another 800mcg 2-3days later if the first dose is not effective. Surgical management may be suggested if bleeding is prolonged(>3weeks) or excessive.

Remember in all pregnant women with vaginal bleeding to check RH status and administer rhogam if RH(-) .OB/GYN consult is required in all women with RPOC. Close follow up should be ensured.

Outcome: ob/gyn was unavailable in house at this community hospital but we discussed with the consultant over the phone. Given the fact that the patient was hemodynamically stable, with her os closed and minimal bleeding, patient was managed medically with 800mcg misoprotol given intravaginally. Patient was given an appointment with OB in 2days and careful discharge instructions.

Stroke Syndromes

In EM2 on February 6, 2011 at 4:05 am

Just a post to remind us of common stroke syndromes.

Remember the homonculus and the circle of willis?

The stroke syndromes are divided by anatomy. Just look at the circle of willis to find the artery, then look at the homunculus to correlate the expected deficit. Remember, right handed people are Left hemisphere dominant and 80% of left handed people are also left hemisphere dominant. Thus only about 20% of people are right hemisphere dominant. If stroke occurs in a non-dominant hemisphere, it will usually manifest as neglect, inattention, agnosia.

Anterior circulation – motor and sensory deficits.

1. Anterior cerebral artery (ACA) stroke –  Motor deficits: contralateral leg, foot, arm paralysis. Sensory deficit: lower>>upper extremities. Loss of frontal lobe control – personality change, gait apraxia, incontinence.

2. Middle cerebral artery(MCA) stroke – most common site of intracranial thrombosis. Motor deficit: contralateral hemiplegia upper extremity weakness > lower extremity; Sensory deficit: contralateral hemianesthesia, aphasia.

3. Posterior cerebral artery (PCA) stroke – PCA supplies the occipital cortex thus a stroke will manifest as loss of vision, cortical blindness, contralateral homonymous hemianopsia, change in mental status, visual agnosia. Ipsilateral cranial nerve 3 palsy

Posterior circulation – ipsilateral cranial nerve deficits + contralateral motor deficits

4. Vertebrobasilar artery stroke – difficult to detect. ipsilateral cranial nerve deficits and cerebellar signs: vertigo, ataxia,nausea/vomitting, vertical/bilateral nystagmus, dysmetria(abnormal finger-nose test), dysdiakokinesis (asking patient to rapidly turn over the fingers and tap the palm with the back of them, repeatedly).

  • Wallenberg Syndrome – Proximal vertebral artery infarct. Lateral medullary syndrome.

5. Basilar artery stroke – ‘locked in syndrome’ – loss of all motor functions asides from upward gaze, +coma.

6. Lacuna Infarct – occlusion of small, perforating arteries of the deep subcortical areas of the brain, cause by small vessel disease from HTN and DM. Presents as pure motor, pure sensory, and ataxic hemiparetic strokes

Singultus

In EM2 on February 6, 2011 at 2:29 am

55yo M s/p recent L craniotomy/Neck Sg in 1/11 for metastatic lung ca to brain presenting with persistent Hiccupps x3days. no resolving, constant. denies any neurological complaints. no focal weakness or numbness.
+Hiccups on exam, neuro exam negative, otherwise well appearing male. CTHead – unchanged, no acute findings, + post-op changes. CXR – redemonstration of LLLobe mass, unchanged.

Outcome: pt given IV torazine 25mg with resolution of symptoms. Hiccups returned, given IV valium 2.5mg with resolution of symptoms. dc’ed home with chlorpromazine rx, f/u with neurosg and PMD.

Teaching point: Treatment of persistent hiccups.

A hiccup is an involuntary, intermittent, spasmodic contraction of the diaphragm and intercostal muscles. A hiccup ’bout’  consists of episodes lasting <48hrs. Persistent hiccups last >48hrs. Intractable hiccups last >1mth.

Differential Dx for persistent/intractable hiccups is extensive. In the patient above, most likey ddx will be vagal nerve irritation from recent surgery or tumor irritating the recurrent laryngeal n.

Treatment – First line is Chlorpromazine – only med thats FDA approved to treat hiccups, (**also the board answer** 🙂 ). IV  better than PO. Dose is 25mg PO TID x7-10days. Remember it may cause dystonic reaction and drowsiness.

Other meds: Metoclopramide, Valium.

High blood pressure

In EM2 on February 3, 2011 at 5:54 am

45yo M presenting for evaluation for high blood pressure. Patient denies any complaints (head or chest pain, shortness of breath, abdominal pain, nausea or vomiting). BP 173/85 on arrival. Chronic hypertensive, non-compliant with medication x1mth, just got his new prescription filled but hasn’t taken any medication.

Outcome: Patient was counseled on negative outcomes of poorly controlled HTN including stroke, renal failure, heart attacks and aortic dissection.

42yo M presenting with severe diffuse HA x 1day, BP 205/100, denies CP,SOB or other complaints. Pt has a history of hypertension, non-compliant with medications. Labs were unremarkable. CTHead negative.

Outcome: Pt was given IV labetalol 10mg – BP reduced to 160/90. Headache was treated symptomatically. Patient improved and was discharged home.

Teaching Point: Management of high blood pressure.

As a frequent complaint in the ED, its important for the EM physician to know when to ‘jump into action’ and when to just offer carefully crafted counseling to will the most unlikely patient into compliance. 😀

Definition: Malignant HTN = diastolic BP>110mmHg + signs of end organ damage.

Malignant HTN and Hypertensive crisis are almost interchangeable. Goal BP control = 25% reduction in MAP(mean arterial pressure) in the first hour and then more slowly after that.

What are your options in terms of medication? You want something titratable i.e an IV medication.

BBlocker – Labetalol (dose 20mg bolus, then 1-2mg/min titrated up), Esmolol (ultra-short acting, typically used to combat reflex tachycardia caused by vasodilators. dose 500µg/kg over 1min, gtt @ 50-100µg/kg/min)

Vasodilator – Nitroprusside (drug of choice in most cases. prolonged use increases risk of cyanide toxicity (an active metabolite. dose 0.25-1µ/kg/min), Nitroglycerin, Hydralazine(traditionally used in pre-eclampsia/eclampsia, may also cause reflex tachy);

AceI – Enalapril;

alpha-blocker – Phentolamine

NOTE in Intracranial Hemorrhage(ICH) – HTN is usually a consequence of ICH but can be as a result. officially, anti-hypertensive medications is NOT indicated and may be harmful in acute stroke syndromes. However clinically, BP control is often initiated to maintain a MAP between 90-110. Remember, too tight a controlled BP in this case may worsen outcome by promoting ischemic damage.

Emergency Drug of Choice
Hypertensive encephalopathy Nitropusside
ICH (intracranial hemorrahge) Labetalol
Cardiac Ischemia Nitroglycerin, Betablocker
Acute pulmonary edema Nitroglycerin
Aortic dissection Nitropusside + BetaBlocker
Preclampsia/Eclampsia Labetalol
Adrenergic Crisis Phentolamine