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READ THAT EKG!

In Uncategorized on December 2, 2011 at 11:48 pm

 

EKG 1 belongs to a 41yo M no PMhx presenting with CP since last Nite. Worse with laying down. Improved with sitting up. Currently having 8/10  CP.

 

EKG 2 belongs to a 50 yr old man presenting with CP x1hour. Onset while doing heavy lifting at home. Actively having CP.

 

Read the EKG and make a decision – to cath or not to cath?! If cath, name the potential culprit lesion.

what am i?!

In Uncategorized on November 9, 2011 at 11:40 pm

What is the diagnosis?!

What is the treatment?!

What is the feared complication?!
w

 

 

answer>>>>>>>>>

Herpes Zoster Ophthalmicus!

Most feared complication – blindness in the affected eye.

Management – PO/IV antivirals (acyclovir), CLOSE OPHTHALMOLOGY FU!

The stroke of insight.

In Uncategorized on September 30, 2011 at 2:09 am

A fascinating TED talk from a neuroanatomist who studied her own stroke as it happened!

 

Abdominal Pain

In Uncategorized on September 12, 2011 at 7:50 pm

 34 yo M with no PMH presents 2/2 diffuse abd pain that began yesterday AM after waking. It has worsened since onset. It is intermittent, pressure-like. No n/v, no f/c, no diarrhea. No urinary sxs. Pain is worse with eating or ambulating. No relief with motrin, maalox, or peptobismol. Pain radaites around to his lower back. Pain is moderately severe. Pt has never had this pain before. Pt also tried a “Mexican medication” for his belly pain with no relief. 

On exam pt appears nontoxic and in no acute distress. RRR heart sounds, Pulm exam CTA b/l, no CVAT, abd exam with mild-moderate epigastric ttp without rebound or guarding, no abd masses.
Labs were ordered.
45mins later, the lab called to state ‘we cannot run the labs because the patient’s blood is ‘milky”
RN was asked to redraw the blood work, and this was noted in the patient’s room.
WHAT IS THE DIAGNOSIS?
 Cholesterol                              666        H      (150-250)        mg/dL
  Result Comment:
 HDL-Cholesterol                          70                                 mg/dL
 Non-HDL Chol (Calc)                      596                                mg/dL
 Direct LDL:                              42                (0-100)          mg/dL
 Triglyceride                             3937
 Lipase                                   44                (13-60)          U/L

IMPRESSION:

Peripancreatic stranding with thickening of the anterior renal and

lateral conal fascia consistent with acute pancreatitis. No

collections identified.

I thought this was a very cool case! The 2 most common causes of pancreatitis are alcohol(35%) or gallstones (40%). Other causes include post-ERCP, trauma, and Infection.

In medical school we learn the other rare but possibly causes – such as hypertriglyceridemia (<1%)! Usually occurring with TG’s >1000. Remember acute pancreatitis doesn’t always present with an elevated lipase (especially if the pancreas is pretty burned out prior to presentation).

REMember – management of acute pancreatitis – NPO, IVF, admit! 

What is wrong with this CT?

In Uncategorized on August 2, 2011 at 11:02 pm

Here’s the scoop… The patient (aka the owner of this CT) is a 60yo M presenting to the ED with acute onset shortness of breath and dyspnea on exhaustion x3days. dyspnea with talking or walking 5 feet with dizziness, nausea and diaphoresis  . denies chest pain, syncope, or lower extremity swelling. Patient states he’s been monitoring his resting HR at home and they’ve ranged from 92-120’s.

PMHx – patient was recently diagnosed with bilateral DVT’s about 3months prior to this presentation. He declined anticoagulation therapy (due to personal beliefs – being a vegan, stating he won’t be compliant with the meds and generally refusing any long term medication therapy). Otherwise no medical history.

FHx – DVT and PE;

ROS – mild conversational dyspnea.
VS: 99.6, 117/82, 98, 18, 97% on RA. PE: patient is in no distress. No rales/rhonchi/wheezing on lung exam. No new murmurs in the heart. RRR. S1/S2. no LE edema. otherwise unremarkable.
DO WE REALLY NEED A CT TO MAKE THIS DIAGNOSIS?!!!!
Teaching Points: Prognosis of untreated non-massive Pulmonary Embolism!

Acute PE is divided into 2 categories – Massive (meaning the patient presents with hypotension – SBP<90mmHh) or Non-massive/submassive (meaning the patient is normotensive – SBP>90mmHg). Submassive PE’s are about 95% of the presenting cases of pulmonary embolism.

Remember your PERC rule Or Well’s criteria for evaluating low-risk PE patients. These rules help you calculate your pretest probability. However, dont forget to include your clinical picture and gestalt in the equation.
We can discuss these rules specifically in another TP but for this case, the PERC rule didnt apply since the patient didnt meet all 8 criteria; Based on Well’s criteria, this patient is at least a moderate-high risk of PE.
Rx.
Lovenox is generally prefered cause of its easier dosing (1mg/kg) however cant be used in patient with renal dysfunction
Heparin is also a choice.
tPa is usually reserved for patient with hemodynamic compromise.
CT read – multiple bilateral pulmonary embolism! Prognosis for this patient….not good (i’m still searching for a more scientific response, with percentages and all. :D)!

Name that poison!

In Uncategorized on July 22, 2011 at 1:31 am

10yo F (otherwise healthy), being managed by dermatology for bilateral lower extremity Molluscum, was scheduled for her Derm appt today to have “Molluscum” of her lower ext removed. Prior to this visit, patient was asked to premedicate her lower extremities with 2.5% EMLA cream and was prescribed (2) 30G tubes. Mum applied the entire 60G 2.5% EMLA cream to both lower extremities and wrapped it with seran wrap 2hours prior to the patients’ appointment. Just before leaving for the appt, patient noted that she felt dizziness. While at the derm office, Pt’s legs became dusky, she became restless and confused. On her mother’s insistence, patient was taken to the nearby ED. Upon arrival, pt was noted to be confused, Oxygen Sats 83-94% while on non re breather, skin looked dusky/grey. Vital signs were otherwise unremarkable.

What poisoning does this child have?

What antidote would you use?

What lab studies are indicated?

Teaching Points: Lidocaine/Methemoglobin toxicity

EMLA is a topical anesthetic made up of Lidocaine + Prilocaine.

Mechanism: These two anesthetics (either individually or in combination) are part of the many drugs that inflict Large oxidative stress on the body and can cause methemoglobinemia. Methemoglobin causes oxygen delivery to tissues to be impaired (by causing oxidation of iron to the ferric state thus reducing the oxygen-carrying capacity of hemoglobin and producing a functional anemia). The oxygen hemoglobin dissociation curve shifts to the left.

Clinical presentation: headache, dyspnea, lightheadedness. Could also lead to cardiac arrhythmia, CNS depression and metabolic acidosis.

Labs:Methemoglobin level, ABG, BMP, Lactate(based on clinical presentation, to look for end-organ damage)

Antidote : Methylene Blue (dose 1-2 mg/kg IV over 5 min. Its effects should be seen in approximately 20 min to 1 h). If ineffective (or if the patient has G6PD and thus is not a candidate for methylene blue), hyperbaric oxygen or exchange transfusion should be considered.

Other interventions: Dermal decontamination (wash the affected skin with skin and water), supplemental oxygen.

Outcome: After discussion with Poison control, it was determined that the patient applied more than 5x the dose of EMLA recommended. Skin was washed off. Labs showed no signs of end organ damage. Methemoglobin level was 15.1mg/dl. Patient was given methylene blue and within 20mins, her dizziness/dyspnea resolved and she regained good color in her extremities. She was admitted overnight for observation.


 

 

 

 

 

 

 

 

Pelvic Mass

In EM3 on July 19, 2011 at 2:00 pm

13yo F presenting with 3days of lower abdominal pain, nausea and vomiting. 5/10 pain at rest, worse with movement or ambulation. LMP 3days ago. Pain was initially felt to be menstral cramps by her dad, but progressively worsened over the course of 3days. Seen by pediatrician and sent to an Outside hospital (OSH) ED for eval.

Vitals: Tmax 100.2 BP109/67 RR 18 100% RA weight -63.4kg.

OSH eval: WBC 13, Hgb 13; CT showed a large 11.2×12.1×8.5cm cystic mass in the middle of the pevis. The cyst was homogenous. Unclear of its origin from the CT thus an US was done. US again re-demonstrated the mass, unclear where the mass was originating from – R ovary was normal, the Left ovary was poorly visualized. Patient was transferred.

Upon arrival to our ED – Patient was a slightly overweight female. On exam, patient was very tender in the LLQ and infra-umbilical area with pain on palpation or movement; the mass was not palpated.  Her pelvic ultrasound was repeated.

What is your differential diagnosis on this patient? – Teratoma, ovarian cyst, ovarian torsion, cancer.

The repeat ultrasound suggest that the mass was likely arising from the left ovary. There was flow seen in the periphery of the mass but no flow demonstrated in the left ovary. The Right ovary was normal size with normal flow.

Teaching Points: Diagnosis of Ovarian torsion

Ovarian torsion – twisting of the ovaries usually due to an abnormality in the adenexa (either a cyst or neoplasm). more common with females that have ovarian hyperstimulation (due to fertility treatments). In young females, can occur in the context of a normal adenexa due to long fallopian tubes.

Classically – patient presents with severe unilateral lower abdominal/pelvic pain over many hours. It IS possible for patient to present with a more prolonged course thus duration of symptoms DOESNOT automatically exclude the possibility of torsion from the differential. Nausea and vomitting is common, fever may be a present but late finding.

Diagnosis is primarily made via Pelvic ultrasound – ovarian enlargement is the most common ultrasound finding. Always ask for dopplers or presence of ‘flow’ in the ovary – the absence of arterial flow may be diagnostic but early in the disease, obstruction of venous flow may be a clue. Some studies suggest an 8hr window (between ovarian torsion and detorsion in the OR) for the ovaries to be salvageable. Thus, time is ovary and even if the patient is out of the 8hr window, this is still a time sensitive diagnosis!

Treatment is surgical detorsion – Gyn or General surgery consult ASAP!

Outcome: necrosis from L fallopian tube to the L ovary were noted on laparoscopy. These were removed. The R ovaries were within normal.

SOB

In EM2 on July 11, 2011 at 1:36 pm
46 yo M c/o L sided CP, intermittent x 3 weeks. Pain is worse with exertion or bending fwd. Associated with shortness of breath  (SOB). Better with some positions.
Vitals: BP-117/82     HR-93      RR-20        92% on RA. 100% on 3L
Labs were all unremarkable and troponin was negative .

CXR on presentation

Old CXR one month prior

How does the new CXR compare to the old?
What bedside maneuver/study can you (the EM resident) perform to make the diagnosis?
What is the difference between a pericardial effusion and pericardial tamponade?
What are the indications for pericardiocentesis in the ED?
What is the technique for performing pericardiocentesis?
Differential diagnosis for a new or worsening pericardiac effusion?
Teaching Points to follow…

How does the new CXR compare to the old?
This is an obvious point BUT Always ‘look at’ and try to read your own images; compare new to old images, call radiology early if something looks suspicious or unclear.
The new CXR was read as: Enlarged cardiac silhouette may represent cardiomegaly and/or pericardial effusion, with small bilateral pleural effusions.
What bedside maneuver/study can you (the EM resident) perform to make the diagnosis?
a bedside ULTRASOUND (US)! never underestimate the usefulness of this tool that is now available in many urban EDs. In a patient presenting with chest pain, shortness of breath and an enlarged cardiac silouhette on CXR, its important to quickly figure out if that silouhette is secondary to an effusion that is ‘potentially’ causing a tamponade and as a result, the patient’s symptoms.
The EM resident in this case did do a bedside Ultrasound: The pericardial sac, myocardium, and 4 chambers were identified. Large circumferential pericardial effusion with some degree of ra and rv diastolic collapse. Enlarged interatrial septum.
Read here for more on the usefulness of bedside US.  

What is the difference between a pericardial effusion and pericardial tamponade?
Think of is this way – an effusion is a noun while tamponade is a verb!
 Normally, the pericardial space contains only about 15-60cc of ultrafiltrate plasma which serves as a lubricant between the visceral and parietal components of the pericardium.
Pericardial effusion is an abnormal accumulation of fluid within the pericardial sac around the heart. Its usually slowly accumulating and patients with effusions are usually asymptomatic. it takes about 200-250cc of pericardial fluid to show up on CXR as cardiomegaly. Effusions can be transudative (due ‘fluid overload’, CHF, hypoproteinemia) or exudative (due malignancy or infection) depending on the etiology.
Cardiac tamponade is the physiologic phenomena that depends most importantly on the rate of fluid accumulation. Tamponade occurs when the pressure in the pericardium is sufficient to overcome and inhibit right ventricular filling, decrease cardiac compliance and thus decrease cardiac output. This happens when fluid accumulates fast within the pericardial sac – faster than the rate of parietal pericardium stretching and faster than the body’s ability to increase blood volume and support RV pressures. The Classic triad we are always taught for Cardiac tamponade is hypotension, muffled heart sounds, and distended neck veins.
EKG typically shows decrease voltage or more rarely, electrical alternans.

Notice every other R wave alternates amplitude. This is due to the change in the size of the R vector being conducted as the heart floats in a large effusion and move away and towards the chest wall (i.e the EKG lead).

Differential diagnosis for a new or worsening pericardiac effusion?
Cancer! Uremia from renal failure, Post infarct myocardial rupture, aortic dissection, iatrogenic cardiac perforation. In trauma, always think penetrating chest injury!
What are the indications for pericardiocentesis in the ED? 
The indication for emergent pericardiocentesis is the presence of life-threatening hemodynamic changes in a patient with suspected cardiac tamponade

What is the technique for performing pericardiocentesis?
Simply performing the classical ‘blind’ subxiphiod approach aiming towards the patient’s left shoulder has HIGH Morbidity and complications (unintentional liver biopsies, gastric perforations, myocardium injury etc) and is really unnecessary with the ever so useful bedside ultrasound!
Check out this website for technique on ultrasound guided pericardiocentesis HERE
Outcome: Cardiology was called to bedside after the bedside ultrasound was performed. US guided pericardiocentesis was performed – 1L of hemorraghic fluid drained. Pericardial window was placed the next day.

this is the patients CXR after the pericardiac drain was placed. If you look closely, you can find the drain on this XR.

Diarrhea, Diarrhea.

In EM3 on July 5, 2011 at 8:30 am

4yo F presents with diarrhea and fever. Patient was seen at the same ED the day prior for fever/vomitting and mild abdominal pain; she was  given zofran with a po challenge which she passed and was sent home. Since home, dad states she’s developed a watery yellow diarrhea, non bloody, about 17bm’s since last night. states she feels tired and has decrease po intake with some diffuse abdominal pain. still making wet diapers. patient is in daycare. no sick contacts. no recent travel.

Vitals: initial T @ 100.8    BP 114/59        HR 165     99% RA       RR 10

GENERAL_APPEARANCE: well_nourished, alert, (+)attentive, (-)smiling, (-)playful, no_acute_distress.

ABDOMEN: normal_BS, soft, mild tenderness in the abdomen (diffuse), (-)guarding, (-)rebound, no_organomegaly, no_abd_masses.

Gastroenteritis was top on the differential. Patient was observed in the ED for about 3hours, PO hydrated and fever controlled with tylenol however there was no significant change in her presentation.She still had diffuse abdominal pain, now more appreciated the in RLQ. Temp spiked to 103.2. Labs were obtained and she was sent to obtain an abdominal ultrasound.

Labs

WBC Count                     22.5      High B/L        (5-11)
Hemoglobin                    12.4               g/dL       (12-14.5)
Hematocrit                    37.2               %          (35-45)
Platelet                      337                B/L        (140-400)
Neutrophils                   76        High %          (25-40)

C-Reactive Protein            15.10     High mg/dL      (0.0-0.8)

Electrolytes were all within normal limits.


What is your diagnosis?

Teaching Point: diagnosis and management of INTUSSUSCEPTION

Definition: invagination of a part of the intestine into itself. Most common around the illeocecal junction. This causes a bowel obstruction.
The tunneled piece of bowel becomes engorged with venous blood and could potentially become ischemic, perforate and cause peritonitis. Etiology is mostly idiopathic (in about 90% of cases). Other causes include viral/ bacterial enteritis, post-op complication or a ‘lead point’ lesion such as a polyp, tumor, meckel’s diverticulum or vascular malformation.

Age: 3 mths to 6yrs old. M>F, more common within the first year of life.

Classic presentation: colicky abdominal pain + currant jelly stool + vomiting -only in 20% of cases. Board exams typically present the case as a child with cyclic abdominal pains in 15-20mins bouts, inconsolable crying, the child drawing the legs up to the chest, or a sausage shaped mass felt in the Right abdomen.

Diagnosis: is typically made via Ultrasound (almost 100% sensitive and specific in the hands of an experienced sonographer). Classic ultrasound findings – bull’s eye” or “coiled spring” lesion. XR abdomen may be useful to look for signs of obstruction or bowel perforation.

Clinical course: most patients recover within 24hours after intervention. However, mortality is close to 100% in 3-4days if there’s no intervention.

Treatment: 3 treatment options:1. Expectant management – with short segments of intussuception. 2. Enema (pneumatic or contrast) 3. Surgical

Contrast enema is diagnostic and therapeutic in approximately 95% of intussusception cases. You’ll need both a pediatric surgeon on stand by and radiologist to perform and interpret the study. About 10% of cases recur within 24hours after successful reduction.  *multiple recurrences hint towards a pathological (rather than idiopathic) cause of the intussusception*. Surgery is indicated when reduction with an enema is incomplete and patient remains symptomatic, or if there are signs of bowel perforation, necrosis or peritonitis.

Disposition: ADMIT!

Outcome: IVF bolus (20mg/kg x2) was given, Morphine was administered for pain cntrol. The patient was transferred to a children’s hospital as the therapeutic contrast enema procedure was not available for pediatrics at this hospital. Ultrasound was repeated at the children’s hospital – showed no signs of intussusception but however diagnosed a perforated appendix. Patient got IV abx and surgery. Did well post-op and was dc’ed home 2days after admission. 

Good way for us all to learn about intussusception I guess! 🙂 

To rhogham or not to rhogam?

In Uncategorized on June 28, 2011 at 3:00 am

29yo F g3p1 about 14wks pregnant by LMP presents after being physically assaulted. Patient states she was in an altercation with another female and was punched multiple times to the abdomen. denies any vaginal bleeding but does note some mild abdominal pain. Vital signs are within normal range for her age. Pelvic exam was unremarkable with no vaginal bleeding.

Bedside  US showed +IUP at about 14weeks with FHR at 130bpm

Labs: rh negative. no Rh antibodies.

Teaching Point: Indications for Rhogam.

Remember! The rh prefix is the name of a surface antigen on RBC’s. Rh negative means those RBCs do not have the antigen. Rh positive means they do. Thus, an Rh negative  person has anti-Rh antibodies! Now, in a pregnant female, this could potentially be a problem if they are pregnant with an Rh+ fetus as the anti-Rh antibodies from the mother could potentially cross the placental and destroy fetal RBC’s IF there is mixing of maternal and fetal blood!.

A woman can be sensitized any time the Rh–positive blood mixes with her blood. This can occur if an Rh–negative woman has once had: Vaginal bleeding during pregnancy, induced or spontaneous abortion, Ectopic pregnancy, chrionic villious sampling or trauma. Once sensitized, it takes approximately one month for Rh antibodies in the maternal circulation to equilibrate in the fetal circulation. In summary:

Rh NEGATIVE = BAD = Sensitization = possible death to current fetus plus issues with future pregnancy, therefore TREAT!

Treatment is Rhogam (anti-Rh IG) 50mcg IM if within the first 20wks or 300mcg IM otherwise.