Intern Report Case 1.5

intern-report

Presented by Maria Pak, MD

HPI

An 11-year-old boy with a PMH of asthma and allergic rhinitis, presents to ED with the chief complaint of right ear pain with drainage and a fever.  Approximately five days prior to being seen in the ED, the patient had a runny nose and nasal congestion.  These symptoms eventually resolved.   However, for the past 2 days, he has been having watery discharge from his right ear, decreased appetite, ear pain, general malaise and subjective fevers.  The discharge worsened on the morning of admission, and his mother felt that he was more tired and not really acting like he normally does (eg more fatigued, not eating right, not as active).  No nausea/vomiting, headaches, neck stiffness, or changes in sensorium.

PMH: asthma, allergic rhinitis, otitis media, eczema
PSH: (Any?) none
FH: sickle cell trait, diabetes, cervical cancer
SH: lives primarily with mother and 3 siblings, and 1 nephew
Meds: albuterol prn, flovent prn, nasonex, loratadine prn
All: NKDA

Physical Exam

Vitals: T 37.1, P130, RR28, BP 121/85, Sat?
Gen: The child is awake, alert, answers questions appropriately and cooperating with the examination.  He is lying on the stretcher,  drowsy but arousable.  Appears to be well-nourished male in no acute distress.
HEENT: Normocephalic, atraumatic.  The neck is supple, with full range of motion and no adenopathy.  The pupils are equal, round, and reactive to light, external structures of the eyes are normal.  Examination of the ears shows an apparent outward displacement of the pinna of the right ear, with tenderness to palpation over the mastoid area on the right.  There is clear fluid coming out of the right ear.  The tympanic membrane on the right is intact, clear and gray, but appears dull.  The tympanic membrane on the left appears normal.  Mucus membranes are moist, but lips are dry.
CV: S1,S2, tachycardic, regular, no murmurs/rubs/gallops
Resp: CTAB, no wheezing/ronchi/rales
Abd: Nontender, nondistended, soft with no organomegaly/masses
Msk: FROM x 4,no tenderness bruising or swelling
Neuro: CN exam: EOMI, patient can close eyes/shrug shoulders/turn head against resistance, sensation intact on both sides of face, visual fields intact, no hearing loss in wither ear.  Strength 5/5 in all extremeties. Patient oriented to person, time, and place.  Gait is normal

Diagnostic Studies

CT: complete opacifaction of right mastoid air cells, middle ear and external auditory canal no evidence of bony destruction or remodeling, opacification of right external canal, lymphoid hypertrophy of adenoids

image2

CBC: wbc 11.1 (53% neutrophils), Hgb 13, plt 290.

Course in the ED
Patient was bloused with 20cc/kg of normal saline.  ENT was consulted, the on call resident recommended Ciprodex ear drops and parenteral clindamycin and ceftriaxone.  He was initially admitted to the PICU due to possible sinus thrombosis seen on CT.  This was later read as negative for thrombosis by a senior radiology attending.  He underwent a right myringotomy by ENT during his hospital stay and wound cultures grew MSSA.  He was treated with antibiotics for 7 days, and then was discharged with a PICC line to have 2 additional weeks of antibiotic therapy at home.

Questions:

1)    What is the most common intracranial complication arising from middle ear infections?
a.    Epidural abscess
b.    Subdural empyema
c.    Meningitis
d.    External carotid artery thrombosis
e.    Petrous apicitis

2)    Which of the following is correct regarding the treatment of acute mastoiditis?
a.    Patients should be made NPO and preoperative laboratory studies should be obtained immediately since the majority of cases require surgical intervention
b.    Antibiotic therapy should always include coverage for anaerobes
c.    In an afebrile patient with stable vital signs and no intracranial complications seen on imaging radiographs, ED discharge with PO antibiotics and close ENT follow-up is appropriate
d.    Initial therapy should include a third-generation cephalosporin or  chloramphenicol with a semisynthetic penicillin, with clindamycin as an option for penicillin allergic patients
e.    Administer topical antibiotics, PO challenge and follow-up with ENT

3)    Other than clinical examination, what is the next most useful diagnostic modality used to diagnose this condition?
a.    MRI
b.    Schuller view radiographs
c.    Myringotomy with tympanocentesis
d.    CT scan
e.    Blood cultures

Please submit your answers to the questions in the “leave a reply” box or click on the “comments” link.  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.

Intern Report Case Discussion 1.4

intern-report

Presented by Devon Moore, MD

Chief Complaint:
She does not voice a specific chief complaint.  She was brought in as a medical code to ED by ambulance from home for “not acting herself”

History:
This is a 59-year-old woman brought into the emergency department as a medical code from home by ambulance.  According to family members, the patient appeared to be confused.  She does not seem to be acting herself, and she is very unsteady on her feet.  This occurred within the past couple of hours.  The patient is conscious but does not seem to be responding appropriately to family members.  On arrival the  patient is alert and oriented to person.  She is able to answer simple questions and follow simple commands.  She denies any complaints of a headache at this time.  No chest pain, difficulty in breathing, abdominal pain, nausea or vomiting.  She denies any extremity-related complaints.  She has had no recent illnesses.

Past Medical, Family, and Social History:
PCP:  The patient does not have a primary care physician.
PMH:  HTN.  It is negative for diabetes, known CAD or stroke.
SH:  Negative.
Meds:  She is not currently on any medications.
FH:  HTN, and negative for diabetes or CAD.
SOCIAL:   She lives with her daughter.  She does not smoke tobacco; consume alcohol or use illicit or I.V. drugs.

Physical Exam:
Vitals: BP was 225/130, HR was 94 and regular, and RR was 18.  Temperature was 36.5.  99% RA

General: She was conscious.  She was alert, but her speech was difficult to understand.  It appears that she may have had either an expressive aphasia, or possibly some mild dysarthria.  She was trying to tell me her name, but it was not understandable.  When asked to take a deep breath, she would open her mouth wide as if to take a deep breath, but she would not breathe deeply.  She did this repeatedly. HEENT: On exam, there was no trauma or abnormality of her scalp. The pupils were about 4mm, round and reactive to light.  EOM were intact; however, she had some element of a nystagmus (not clearly horizontal or vertical).  It may be rotary.  Her fundi looked to have a slight indistinctness of her left fundus and optic disc.  There was no obvious hemorrhage.  Her right optic disc was sharp without any obvious hemorrhage.  Her mouth was without intraoral lesions, and she had a positive gag reflex.  Her neck was supple with no nuchal rigidity.  No meningismus.  Trachea was midline without deviation.   Carotids were 2+ and without bruits.  No JVD.
RESPIRATORY: CTA bilaterally, with no rales or wheezes.  She was not cyanotic or diaphoretic.  No accessory muscle use.
CARDIAC: normal S1 and S2.  No S3 or S4 gallops.  No murmurs or rubs.  Good distal pulses.  Chest wall was non-tender.
ABDOMEN: negative.
MUSCULOSKELETAL: good pulses, no acutely inflamed joints.  Symmetric muscular strength and tone, and is able to move her extremities distally.
NEUROLOGIC: awake, alert and oriented to person.  No obvious sensory deficits to soft touch.  Deep tendon reflexes were hyper-reflexic.  Patella and Achilles were 3+.  She had clonus of both lower extremities and a slightly up-going toe on the left.  She had a downward plantar response on the right.  She had dysmetria seen with the left hand (right not tested).  Gait not tested, but when transferring her from EMS bed to resuscitation bed, she was uncoordinated and constantly fell on her left side while trying to “scoot” to the left to the next bed.

Labs:
•    Accu-check was 192

Diagnostic Studies:
•    12-lead-EKG showed normal sinus rhythm at 87 bpm, normal axis, no ventricular ectopy, normal PR, QRS, and QT intervals.   A voltage criterion for LVH is met.
•    Single-view CXR did not show any evidence of infiltrate, pneumothorax, or effusion.  There was no significant cardiomegaly.

Questions:

1.    Which of the following would be the next most appropriate steps to take to make a diagnosis?
a.)     CBC, lytes, BUN, cr, U/A, UDS and SDS
b.)     Aortic angiography
c.)     TSH
d.)     CT Head
e.)     Plasma metanephrine testing, MRI abdomen

2.    Which is the most appropriate in management of this patients’ blood pressure?
a.)     I.V. vasodilators and/or adrenergic antagonists for rapid reduction in BP to obtain a normal level  (<140/90)
b.)    Maintain SBP <160 mm Hg, and give oral nimodipine
c.)    Reduce mean arterial pressure (MAP) up to 20-25% over the first hour of treatment, use short acting and titratable agents I.V., with constant patient monitoring
d.)    I.V. Alpha-adrenergic antagonist therapy only to reduce BP
e.)    SBP <160, DBP <110, and I.V. magnesium sulfate

3.)  Which of the following is most closely associated with the term ‘hypertensive emergency’?
a.)  SBP >200, DBP >120
b.)  SBP >200, DBP >120 with pre-existing conditions (CHF, CAD, Renal insufficiency)
c.)  acute end-organ damage
d.)  longstanding, poorly controlled HTN
e.)  papilledema

Case Discussion

According to the Joint National Committee (JNC-7), the classification system for hypertension is the following:
•    Prehypertension – Systolic blood pressure (SBP) 120-139mmHG or diastolic blood pressure (DBP) 80-89 mmHG
•    Stage I hypertension – SBP 140-159mmHg or DBP 90-99mmHg
•    Stage II hypertension – SBP >160 mmHg or DBP >100 mmHg
•    Stage III hypertension – SBP ≥180mmHg or DBP ≥ 110 mmHg¹

This guide is an estimate used for the basis of a treatment guideline in those who are asymptomatic, and without evidence of organic pathology.  There are many other factors to look at based on co-existing conditions.  In general, those in stage I should be on 2 antihypertensive, and those in stage II should be on 2 antihypertensive medications.

When looking at our case, we had a woman over the age of 55 with a known history of HTN.  When I checked her blood pressure, it was 225/130.  This is enough to raise an eye-brow and realize that this is acutely too high.  But what was more alarming with her picture is that she portrayed evidence of an altered mental status.  Her family said that she was “acting different,” and we also witnessed this during our physical examination.

Transient Hypertension
This is seen with other conditions such as anxiety, alcohol-withdrawal syndromes, sudden cessation of medications, and some toxicologic substances².  Treat the underlying cause.

Acute Hypertensive episode
This is considered stage III hypertension without signs or symptoms of impending target-organ damage².  Controversy exists for treatment in this category.

Hypertensive Urgency
Many physicians will tell you that there is really no such thing as “hypertensive urgency” because it doesn’t have much utility in practice.  It represents a risk for imminent target-organ damage, but it is all relative.  This is especially true in our practice because many of our patients don’t have (or don’t utilize) primary care physicians for regular check-ups and control of conditions.  This means that someone who has high blood pressure could have had it for many years without knowing; and that is the danger (silent killer).  Hypertensive crises affect less than 1% of hypertensive adults in the United States.

Hypertensive Emergency
This term is most closely associated with target-organ, or acute end-organ damage.  It encompasses a spectrum of clinical presentations where uncontrolled BP’s lead to end-organ dysfunction.  These include the following:

Neurological

o    Hypertensive encephalopathy
o    Cerebral vascular accident/cerebral infarction
o    Subarachnoid hemorrhage
o    Intracranial hemorrhage

Cardiovascular

o    Myocardial ischemia/infarction
o    Acute left ventricular dysfunction
o    Acute pulmonary edema
o    Aortic dissection

Other

o    Acute renal failure/insufficiency
o    Retinopathy
o    Eclampsia
o    Microangiopathic hemolytic anemia³

When reviewing the above, it seems that our patient fits most with the picture of a hypertensive emergency.  Because of the cerebellar features that were consistent with our physical exam, our suspicions should be raised for a neurological problem.  The next best test for diagnosing purposes would be imaging, looking for any intracranial process such as stroke or hemorrhage.  CT head without contrast is a practical choice.

CT head without contrast was read as the following:

1.) Large area of hemorrhage in the posterior fossa, greater in the right cerebellar hemisphere compared to the left.  There is effacement of the fourth ventricle and the brainstem in this region.  2.) Chronic small vessel ischemic disease.  3.) Remote infarcts in the midbrain.

Laboratory results are still an important part of the presentation, because they can clue one in to other evidence of organ function, such as renal impairment.  They can clue one in to certain ingestions (sympathomimetics, cocaine).  And if the clinical picture fits, they can clue one in to other less common etiologies for elevated blood pressure (i.e. thyroid disease, pheochromocytoma).  But if you rely only on the labs, they may not be helpful at all.

Laboratory Results:
K+ hemolyzed >8.0; other lytes within normal limits.  Accu-check is 192.  CBC is normal with no sign of coagulopathy.  SDS and UDS are completely negative.  UA is negative for infection, or protein.

When discussing treatment options, it is important to stay aware that someone presenting in a state such as this may have a failure of their normal autoregulation.  Cerebral autoregulation is the ability of the cerebral vasculature to maintain a constant cerebral blood flow (CBF) across a wide range of perfusion pressures.  Patients with chronic hypertension can tolerate higher mean arterial pressures (MAP) before they have disruption of their autoregulation system. However, such patients also have increased cerebrovascular resistance and are more prone to cerebral ischemia when flow decreases, especially if blood pressure is decreased into normotensive ranges.  Rapid rises in blood pressure can cause hyperperfusion and increased CBF, which can lead to increased intracranial pressure and cerebral edema.   Because of this, certain antihypertensive treatments can exacerbate these problems.

The most practical agents to use in this setting are those that are more short acting, and titratable through the I.V. route.  The goal should be to lower the mean arterial pressure (MAP) by no more than 20-25% within the first hour.  Chronically hypertensive patients can develop symptoms of brain hypoperfusion if their blood pressure is lowered to what is defined as a normal level.  The “normal” level may be below the limits of an individual’s adjusted autoregulation (about 25% below a patient’s baseline MAP).

Sodium nitroprusside is the medication of choice, but nitroglycerin and labetalol are also successfully used.  In regards to question #2, choice b would be used for a subarachnoid hemorrhage (SAH), choice d would be used with acute cocaine precipitated HTN, and choice e involves the world of obstetrics and gynecology.

Answers:

1. D

2. C

3. C

Click Here for an excellent review

References

1.    Joint National Committee (JNC) on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure
2.    Emergency Medicine: a comprehensive study guide, Tintinalli.  Sixth edition
3.    Emedicine: Hypertension

Intenr Report Case 1.4

intern-report

Presented by Devon Moore, MD

Chief Complaint:
She does not voice a specific chief complaint.  She was brought in as a medical code to ED by ambulance from home for “not acting herself”

History:
This is a 59-year-old woman brought into the emergency department as a medical code from home by ambulance.  According to family members, the patient appeared to be confused.  She does not seem to be acting herself, and she is very unsteady on her feet.  This occurred within the past couple of hours.  The patient is conscious but does not seem to be responding appropriately to family members.  On arrival the  patient is alert and oriented to person.  She is able to answer simple questions and follow simple commands.  She denies any complaints of a headache at this time.  No chest pain, difficulty in breathing, abdominal pain, nausea or vomiting.  She denies any extremity-related complaints.  She has had no recent illnesses.

Past Medical, Family, and Social History:
PCP:  The patient does not have a primary care physician.
PMH:  HTN.  It is negative for diabetes, known CAD or stroke.
SH:  Negative.
Meds:  She is not currently on any medications.
FH:  HTN, and negative for diabetes or CAD.
SOCIAL:   She lives with her daughter.  She does not smoke tobacco; consume alcohol or use illicit or I.V. drugs.

Physical Exam:
Vitals: BP was 225/130, HR was 94 and regular, and RR was 18.  Temperature was 36.5.  99% RA

General: She was conscious.  She was alert, but her speech was difficult to understand.  It appears that she may have had either an expressive aphasia, or possibly some mild dysarthria.  She was trying to tell me her name, but it was not understandable.  When asked to take a deep breath, she would open her mouth wide as if to take a deep breath, but she would not breathe deeply.  She did this repeatedly. HEENT: On exam, there was no trauma or abnormality of her scalp. The pupils were about 4mm, round and reactive to light.  EOM were intact; however, she had some element of a nystagmus (not clearly horizontal or vertical).  It may be rotary.  Her fundi looked to have a slight indistinctness of her left fundus and optic disc.  There was no obvious hemorrhage.  Her right optic disc was sharp without any obvious hemorrhage.  Her mouth was without intraoral lesions, and she had a positive gag reflex.  Her neck was supple with no nuchal rigidity.  No meningismus.  Trachea was midline without deviation.   Carotids were 2+ and without bruits.  No JVD.
RESPIRATORY: CTA bilaterally, with no rales or wheezes.  She was not cyanotic or diaphoretic.  No accessory muscle use.
CARDIAC: normal S1 and S2.  No S3 or S4 gallops.  No murmurs or rubs.  Good distal pulses.  Chest wall was non-tender.
ABDOMEN: negative.
MUSCULOSKELETAL: good pulses, no acutely inflamed joints.  Symmetric muscular strength and tone, and is able to move her extremities distally.
NEUROLOGIC: awake, alert and oriented to person.  No obvious sensory deficits to soft touch.  Deep tendon reflexes were hyper-reflexic.  Patella and Achilles were 3+.  She had clonus of both lower extremities and a slightly up-going toe on the left.  She had a downward plantar response on the right.  She had dysmetria seen with the left hand (right not tested).  Gait not tested, but when transferring her from EMS bed to resuscitation bed, she was uncoordinated and constantly fell on her left side while trying to “scoot” to the left to the next bed.

Labs:
•    Accu-check was 192

Diagnostic Studies:
•    12-lead-EKG showed normal sinus rhythm at 87 bpm, normal axis, no ventricular ectopy, normal PR, QRS, and QT intervals.   A voltage criterion for LVH is met.
•    Single-view CXR did not show any evidence of infiltrate, pneumothorax, or effusion.  There was no significant cardiomegaly.

Questions:

1.    Which of the following would be the next most appropriate steps to take to make a diagnosis?
a.)     CBC, lytes, BUN, cr, U/A, UDS and SDS
b.)     Aortic angiography
c.)     TSH
d.)     CT Head
e.)     Plasma metanephrine testing, MRI abdomen

2.    Which is the most appropriate in management of this patients’ blood pressure?
a.)     I.V. vasodilators and/or adrenergic antagonists for rapid reduction in BP to obtain a normal level  (<140/90)
b.)    Maintain SBP <160 mm Hg, and give oral nimodipine
c.)    Reduce mean arterial pressure (MAP) up to 20-25% over the first hour of treatment, use short acting and titratable agents I.V., with constant patient monitoring
d.)    I.V. Alpha-adrenergic antagonist therapy only to reduce BP
e.)    SBP <160, DBP <110, and I.V. magnesium sulfate

3.)  Which of the following is most closely associated with the term ‘hypertensive emergency’?
a.)  SBP >200, DBP >120
b.)  SBP >200, DBP >120 with pre-existing conditions (CHF, CAD, Renal insufficiency)
c.)  acute end-organ damage
d.)  longstanding, poorly controlled HTN
e.)  papilledema

Please submit your answers to the questions in the “leave a reply” box or click on the “comments” link.  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.

Intern Report Case Discussion 1.3

intern-report

CASE

Discussion

This case unfolded in such a way that it really invoked critical thought and differentials in my mind. I worked with my attending and the tox consultant to “best guess” my way through his care—trying to make a diagnosis based on response to treatment. It was really interesting to me and I learned much about the presentation and treatment of an overdose of these classes of drugs while seeing it all happen in front of me. So, there are many “correct” answers to the questions posed. The one keyed as correct is a reflection of the situation as it was at that time and thought to be the best choice based on that. I’m sure all of the very intelligent members of my class have comments about the varying degrees of how right and wrong each answer is to these questions and that’s great! I hope it inspired as much thought in the critique of answers as it did in me while working through it in the ED.

1.) Based on this patient’s clinical presentation, which of the following would be the most likely medication/class of drug suspected as an overdose?
a.) beta blocker
b.) calcium channel blocker
c.) clonidine
d.) digoxin
e.) glipizide

Here are the key elements  in this patient for this question:
He had no improvement in his mental status or hemodynamics with Narcan. He had no notable PVC’s or characteristic “swoop” of digoxin on EKG and his QRS complexes were wide, not narrow. He had no resolution of his bradycardia with D50 in the field. He presented with cool extremities and a low body temperature.

DIFFERENTIAL DIAGNOSIS — Many drugs can cause profound hypotension or bradydysrhythmia in overdose. Calcium channel blockers, digoxin, clonidine, and cholinergic agents must be considered when evaluating bradydysrhythmia potentially caused by a toxic ingestion.

Calcium channel blockers are less likely than beta blockers to produce alterations in mental status, and frequently do not do so unless the patient is in profound shock. Hyperglycemia occurs more often with calcium channel blocker toxicity, while beta blockers are associated with hypoglycemia.

Nausea and vomiting occur more often with digoxin toxicity than beta blocker toxicity. Digoxin may cause characteristic changes in an electrocardiogram, such as scooped ST segment depressions. Digoxin is more likely to produce rhythms of increased automaticity, such as atrial tachycardia with atrioventricular block, premature ventricular contractions, or ventricular arrhythmias.

Clonidine produces a constellation of signs that can resemble opioid overdose, including somnolence and miosis, but are accompanied by hypotension and bradycardia.

Overdose of a cholinergic agent can present with bradycardia but also includes other characteristic features (salivation, lacrimation, urination, defecation, GI upset, and muscle excitability).
Overdose of diabetic medications would most likely be reversed by intravenous glucose administration and would not cause persistant bradydysrhythmia.

2.) While considering all clinical information in this case, which of the following clinical findings helps to identify the most likely overdosed medication?

a.) core body temperature
b.) electrocardiogram findings
c.) mental status
d.) peripheral pulses / capillary refill
e.) serum glucose values

Key considerations here:
A low body temperature can be just a reflection of the environment. It is not specific. EKG findings are rarely specific to one exact drug and bradycardia can develop for many reasons.

A person’s mental status can be altered by medications, but it will be altered if a patient is not perfusing their brain well as in the case of significant hypotension.

A diminished capillary refill will be present in any hypotensive patient when compensatory mechanisms try to preserve central blood flow.

This patient is not a diabetic. He required many boluses of glucose. He was found with an empty bottle of medication for “high blood pressure”.

Physical findings — Most patients who overdose on beta blockers become symptomatic within two hours following ingestion, and nearly all develop symptoms within six hours. Exceptions to this general rule include ingestions of sustained release medications and sotalol. In these cases, delayed toxicity up to 24 hours after ingestion can occur. Bradycardia and hypotension are the most common effects, and in severe overdoses can result in profound myocardial depression and cardiogenic shock. Ventricular dysrhythmias are seen more frequently following propranolol and acebutolol exposures, probably because of the increased membrane-stabilizing activity (MSA) of these agents. Other potential effects of severe toxicity include mental status change, seizure, hypoglycemia, and bronchospasm.

Mental status changes, including delirium, coma, and seizures, occur most frequently in patients with severe hypotension, but can occur in those with normal blood pressure. Similarly, respiratory depression usually occurs in hypotensive, comatose patients, but has been reported in awake patients. Specific agents, particularly propranolol, are associated with neurologic effects in the absence of cerebral hypoperfusion.

Patients with severe peripheral vascular disease described a variety of complications including worsening claudication, cold extremities, absent pulses, and, in some cases, cyanosis and impending gangrene. Raynaud’s phenomenon can also be a manifestation of nonselective beta blockade. It was thought that both the reduction in cardiac output and blockade of beta-2-receptor-mediated skeletal muscle vasodilation contribute to the vascular insufficiency.  Beta blockers with beta-1 selectivity or ISA do affect the peripheral vessels to the same degree as the nonselective drugs.

Electrocardiogram — Beta blockers decrease conduction velocity across the atrioventricular (AV) node, resulting in PR prolongation; they also slow automaticity within the sinoatrial (SA) node, causing bradycardia. In severe poisoning, the electrocardiogram can show ANY bradydysrhythmia, and can progress to asystole.

Following overdose, manifestations of toxicity are observed in varying degrees, depending on the specific agent and dose involved. In addition to beta-adrenoreceptor blockade, three properties that affect toxicity include the membrane stabilizing activity (MSA), lipophilicity, and intrinsic sympathomimetic activity (ISA) of the ingested agent.

•    Membrane stabilizing activity (MSA) – Membrane stabilizing agents (eg, propranolol, acebutolol) inhibit myocardial fast sodium channels, which can result in a widened QRS interval and may potentiate other dysrhythmias.

•    Lipophilicity – Beta blockers with high lipid solubility (eg, propranolol) rapidly cross the blood brain barrier into the central nervous system, predisposing to neurologic sequelae such as seizures and delirium.

•    Intrinsic sympathomimetic activity (ISA) – Many agents demonstrate a partial agonist effect at the beta receptor site, resulting in less bradycardia and hypotension in therapeutic and supratherapeutic doses. Bronchoconstriction is also less likely to occur with compounds that possess intrinsic sympathomimetic activity (ISA), or beta-1 selectivity. However, the protective effects of ISA do not completely prevent cardiovascular toxicity following intentional or accidental overdose.

3.) Once the patient is stabilized, what treatment should be initiated and was recommended by poison control?
a.) activated charcoal
b.) calcium infusion
c.) continuous intravenous hydration
d.) hemodialysis
e.) whole bowel irrigation

Key points in this question:
We don’t know the time interval between ingestion and presentation.
A patient in resus always has fluids running, but you need to remember to look up and take stock in just how much fluid they are getting. A 49 year old hypertensive male probably has some LV dysfunction and may not benefit from liters of fluid.

First things first…the usual O2, IVF, give D50 for any further low blood sugars and address the bradycardia and hypotension.

Treat hypotension with intravenous (IV) boluses of isotonic fluid; treat symptomatic bradycardia with atropine. Atropine is given in a dose of 0.5 to 1 mg every 3 to 5 minutes up to a total of 0.03 to 0.04 mg/kg.

IV fluid and atropine often do not completely reverse the cardiotoxic effects of beta blocker overdose. In such cases, add the following treatments in succession based upon patient response:
•    Glucagon
•    IV calcium salts
•    Vasopressors
•    High dose insulin and glucose infusions
•    Phosphodiesterase inhibitors

Treatments
Glucagon — Despite limited data, glucagon is considered first-line, antidotal treatment for beta blocker overdose [13,14]. Intravenous (IV) glucagon is given as a slow bolus dose followed by continuous infusion. An initial bolus of 5 mg intravenously is administered over one minute; if there is no increase in pulse or blood pressure after 10 to 15 minutes, a second bolus should be administered. The initial pediatric dose is 50 micrograms/kg. An effect should be observed within 1 to 3 minutes, with a peak response at 5 to 7 minutes. If there is no observed effect after 10 minutes following a second dose, it is unlikely an infusion will provide benefit.

If there is an increase in pulse or blood pressure, an infusion is started at a rate of 2 to 5 mg/hour (pediatric dose 70 micrograms/kg/hour). The goal is to maintain a mean arterial pressure of 60 mmHg. If this cannot be achieved, additional therapies are implemented in a sequential manner, beginning with calcium salts. When used as a sole agent in humans, glucagon has been associated with treatment failures.
Vomiting is common following administration of glucagon.

Glucagon activates adenylate cyclase at a site independent from beta-adrenergic agents, causing an increase in adenosine 3′-5′-cyclic monophosphate (cAMP). Elevations in cAMP increase the intracellular pool of calcium available for release during depolarization, augmenting contractility. The successful use of glucagon to manage beta blocker toxicity has been documented in many case reports, but no controlled trials involving humans have been conducted. One review of the available controlled trials in animal models found that glucagon increased heart rate (HR), at least transiently, but had minimal effect on mean arterial pressure (MAP).

In 2006, a trial comparing vasopressin with glucagon in a swine model of propranolol overdose found no difference in survival at 4 hours. No difference was detected in HR, MAP, systolic BP, or cardiac output, except in the first hour, when vasopressin caused a marked increase in MAP and systolic BP. Notably, cardiac output did not improve following glucagon administration.

Calcium — A number of case reports demonstrate the efficacy of IV calcium salts in treating beta blocker toxicity. Either calcium chloride or calcium gluconate may be given.
Calcium chloride, 1 g of a 10 percent solution (10 mL), is given as a slow push, and should be administered via a central venous catheter. The dose may be repeated up to a total of 3 grams. The pediatric dose is 20 mg/kg (maximum dose is 1 g); up to 60 mg/kg may be given.

Calcium gluconate should be utilized if only peripheral IV access is available. The percentage of elemental calcium in calcium gluconate is one-third that of the calcium chloride salt, so 30 mL of a 10 percent solution should be administered as an initial dose. In children, give 60 mg/kg per dose (maximum dose is 3 g).

IV calcium salts may improve hemodynamic parameters by increasing inotropy. Animal models suggest that calcium salts increase blood pressure and cardiac output, but do not increase heart rate, following combined calcium channel blocker and beta blocker overdose.

Glucagon — Glucagon increases intracellular levels of cyclic AMP and, in animal models, has been shown to increase heart rate in calcium channel blocker toxicity [16]. It has minimal effects on the mean arterial pressure, however. Glucagon has been effective in treating human cases of CCB toxicity

Catecholamines — In animal models and human case reports, treatment of beta blocker overdose with catecholamine infusion alone has resulted in poor outcomes. One study of insulin therapy in propranolol toxicity was terminated early when every pig in the insulin and glucose treatment group achieved the study goal of 4 hour survival, while those treated with vasopressin and epinephrine died within 90 minutes [22]. Cardiac output (CO) in animals treated with insulin and glucose increased throughout the trial; CO in animals treated with vasopressin and epinephrine decreased until death.

Hypoglycemia must be corrected prior to initiating insulin therapy. We begin treatment in adults by administering 50 mL of 50 percent dextrose (D50W) IV, followed by an insulin bolus of 2 units/kg over 5 minutes. An insulin infusion is then started at 0.5 units/kg/hour, with a goal rate of 2 units/kg/hour. A dextrose infusion of 1 g/kg/hour is begun simultaneously.

The pathophysiology of beta-blocker intoxication is similar in many respects to that of calcium channel blocker (CCB) intoxication, for which high dose insulin and glucose has been more extensively studied. Although the mechanism is not completely understood, both CCB and beta blocker poisoning appear to interfere with myocyte metabolism. In addition, beta blockers inhibit pancreatic insulin release further reducing available glucose and diminishing CO. Insulin appears to improve inotropy by providing substrate for aerobic metabolism within the myocyte.

Though the mechanism is not completely understood, CCBs appear to disrupt fatty acid metabolism and create relative insulin resistance within the myocardium. This state of carbohydrate dependence and insulin resistance can theoretically be overcome with high-dose insulin [20]. Animal studies of CCB toxicity have shown improved survival associated with hyperinsulinemia/euglycemia therapy compared with calcium, epinephrine, or glucagon [21,22]. Clinical experience with this approach is limited [23,24]; in one case series of four verapamil-poisoned patients, hyperinsulinemia/euglycemia therapy improved blood pressure and ejection fraction without changing heart rate [23]. High-dose insulin therapy is also used in beta blocker poisoning.

Gastrointestinal (GI) decontamination — GI decontamination may involve activated charcoal (AC), whole bowel irrigation, or gastric lavage; therapy is based upon clinical circumstance. (See “Decontamination of poisoned adults”).
We suggest treatment with activated charcoal (AC), 1 g/kg by mouth or nasogastric tube, in all patients who present within 1 to 2 hours of a known or suspected beta blocker ingestion, unless there are contraindications to its administration. Charcoal should be withheld in patients who are sedated and may not be able to protect their airway, unless endotracheal intubation is performed first. However, endotracheal intubation should not be performed solely for the purpose of giving charcoal.
Asymptomatic patients who present more than two hours after a reported ingestion are unlikely to benefit from AC, and we do not recommend routine treatment in these patients.

The role of activated charcoal in symptomatic patients who present several hours after ingestion is more controversial. We suggest the administration of AC (1g/kg by mouth or nasogastric tube) if there are no contraindications to charcoal administration. Although there are no data to suggest improved outcomes with AC in such patients, we believe that AC is a relatively safe intervention whose potential benefits in this situation outweigh its risks.
Gastric lavage should not be routinely performed, but may be considered for patients who present within one hour following ingestion of a large quantity of medication. Large sustained or controlled release tablets may not pass through the oral gastric tube.

Whole bowel irrigation is reserved for patients who have ingested sustained release or enteric coated preparations, or have suspected drug concretions (pharmacobezoars) in the GI tract.

Other therapies
•    Sodium bicarbonate — Sodium bicarbonate has been used successfully in the treatment of beta blocker induced arrhythmia [26,27]. Because it is a relatively safe intervention, we suggest giving it as an adjunct for patients with QRS widening.
The dose of sodium bicarbonate is 1 to 2 mEq/kg given as an IV push, which may be repeated. If treatment is effective, an infusion can be started. We mix 132 mEq of sodium bicarbonate in 1 liter of D5W and infuse at 250 mL/hour in adults, and at twice the maintenance fluid rate in children. The infusion is tapered once the arrhythmia resolves. (See “Tricyclic antidepressant poisoning”).
•    Magnesium — Magnesium may be administered when ventricular arrhythmias are present or hypomagnesemia is suspected. Sotalol has a high propensity to induce ventricular arrhythmias and will often require magnesium, administered as a 2 g IV bolus or as a continuous infusion.
•    Intravenous pacing — Ventricular pacing may be effective in patients with profound bradycardia, or in patients with combined beta blocker and calcium channel blocker intoxication [28]. However, ventricular pacing frequently fails to capture, or increases the heart rate without a corresponding increase in perfusion [29]. IV pacing can be implemented if there is no response to pharmacologic therapies, and the patient remains bradycardic and hypotensive. Some authors note a decrease in blood pressure with pacing [4]. (See “Temporary cardiac pacing”).
•    Intraaortic balloon pump — The intraaortic balloon pump has been used successfully after failure of pharmacologic management in severe cases of propranolol and atenolol overdose [30,31] and in combined verapamil-SR (sustained release) and atenolol overdose [32]. (See “Intraaortic balloon pump counterpulsation”).
•    Hemodialysis — Hemodialysis has a minimal role in the treatment of beta blocker overdose and is effective only with hydrophilic, minimally protein-bound beta blockers such as atenolol [33]. Nadolol, sotalol, acebutolol, and atenolol are reportedly removed by hemodialysis, but metoprolol, propranolol, and timolol are not.
Hemodialysis is reserved for patients who have not improved despite aggressive medical intervention, have ingested a significant amount of a beta blocker that can be removed using dialysis (eg, acebutolol), or have ingested other cardioactive medications that may exacerbate toxicity. In such cases, the emergency clinician should contact a nephrologist early in the patient’s course to avoid delays in preparing for hemodialysis.

Continuous venovenous hemodialysis (VVHD) can be used if the patient is not able to tolerate traditional hemodialysis due to pronounced hypotension. The decision to initiate hemodialysis and the selection of the appropriate type is made in consultation with the nephrologist.

References:

Will post soon.

Intern Report Case 1.3

intern-report

History of Present Illness

A 49-year-old male is brought by EMS as a medical code to resuscitation.  He was apparently found by police lying in the street.

EMS reports an initial rapid glucose of 32 mg/dL, which improved to 56 mg/dL with 1 amp of D50 and to 79 mg/dL following a second amp of D50.  EMS noted an empty medication bottle near the patient, and only the words “to treat hypertension” could be made out on the label.  EMS believes that they recognize this patient and have transported him many times in the past with seizure disorder, noncompliant with meds. EMS did not witness any seizure activity during their assessment and transport.

Review of systems not able to be obtained at this time.

PMHx: Per EMS, seizure disorder and apparently hypertension.
PSHx: Unknown
Meds: The patient does not know their names.
ALLERGIES: NONE per patient.
SocHx: Denies illicit drug use, or alcohol use today.
FHx: Unknown.

Physical Exam
Vital signs on arrival to resuscitation:  BP 90s/60s, P 30s, Respiratory rate varies with alertness, but never over 16, T 34.0 rectally.  Pulse oximetry unable to be obtained as the patient is very cold.

On arrival to resuscitation the patient appeared disheveled and was somnolent, fully immobilized, wearing multiple layers of clothing.  He opened his eyes to verbal command, spontaneously moved all 4 extremities and had no obvious signs of trauma.

HEENT: There are no obvious lacerations, contusions or depressions palpated on his scalp.  Pupils were 2 mm and minimally reactive.  Mucous membranes were moist.
Neck: The C-collar was left in place due to the patient not being awake enough to ascertain spinal tenderness.  The trachea is midline and there is no JVD.
Respiratory: There is a slight amount of wheezing in the left lung.
Cardiac: Heart sounds are distant.
Gastrointestinal: Abdomen is soft and scaphoid.  There is no palpable tenderness or appreciable rebound tenderness.  Pelvis is stable. Extremities:  No abrasions, deformities, or edema.  Peripheral pulses are not readily palpable, the extremities are cold to the touch.
Skin: Cool and dry to the touch without rashes or lesions.
Neurological: GCS is 13 (E3, V4, M6), motor 5+/5+ in all extremities.

Initially in resuscitation, he was placed on supplemental oxygen, a cardiac monitor showed a wide complex bradycardia with a rate in the 30s to 50s, two large bore IV’s were established.  The patient was observed to have periods of apnea for which naloxone 2 mg. IV push was given, which had little clinical effect.  His initial accucheck blood sugar was 171 mg/dL.

While the ER staff attempted to verify his identity to review CIS, a 12-lead EKG was obtained and is shown here.

ekg3

A portable chest x-ray was also obtained and was interpreted as normal.

Questions

1. Based on this patient’s clinical presentation, which of the following would be the most likely medication/class of drug suspected as an overdose?
a.    beta blocker
b.    calcium channel blocker
c.    clonidine
d.    digoxin
e.    glipizide

2. While considering all clinical information in this case, which of the following clinical findings helps to identify the most likely overdosed medication?
a.    core body temperature
b.    electrocardiogram findings
c.    mental status
d.    peripheral pulses / capillary refill
e.    serum glucose values

3. Once the patient is stabilized, what treatment should be initiated and was recommended by poison control?
a.    activated charcoal
b.    calcium infusion
c.    continuous intravenous hydration
d.    hemodialysis
e.    whole bowel irrigation

______________________________________________________________________________
Please submit your answers to the questions in the “leave a reply” box or click on the “comments” link.  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.

Intern Report Case Discussion 1.2

intern-report

Presented by Jeff McMenomy, MD

History of Present Illness:
A 75-year-old woman is brought to the Emergency Department by EMS. Her family states the patient complained of gradually worsening generalized weakness and decreased responsiveness over the course of the previous week.  They also state that she is “not being herself”.  EMS noted the patient to be minimally responsive, bradycardic, and hypotensive en route to the hospital.

PMHx: hypertension
PSHx: unknown
FHx: unknown
SocHx: unknown
Allergies: codeine, penicillin
Medications: unknown

Physical Exam

Vitals: T 36.2 C, HR 40, BP 86/43, RR 18, O2 97% on 15 L nonrebreather
Gen: obtunded, oriented x 1, responds to name but not oriented to place or time
HEENT: NC/AT, PERRL, EOMI, no conjunctival pallor, TMs clear b/l, mucous membranes dry, no tonsillar exudates or erythema, + gag reflex
Neck: supple, FROM, no JVD, trachea midline, no cervical LAN
Heart: bradycardic, regular rhythm, no murmurs, rubs, or gallops.
Lungs: clear to auscultation b/l in all fields, no wheezes/rales/rhonchi, normal respiratory effort
Abdomen: soft, nontender, nondistended, bowel sounds normoactive, no rebound/masses/guarding
Vascular: capillary refill 3 seconds, pulses thready but palpable in all four extremities.
Neuro: responds to her name, follows commands. Eyes open spontaneously.  Tongue and uvula are midline.  Moving all four extremities.
Skin: + mild diaphoresis, no rashes

Electrocardiogram:

ecg1

QUESTIONS:

1. Given this patient’s overall clinical picture, what would be the most appropriate initial course of action?

A.   Place patient on a monitor, establish IV access, and administer 0.5 mg doses of atropine while preparing for transcutaneous pacing.

B.   Place patient on a monitor, establish IV access, and administer 325 mg of aspirin, 0.4 mg nitroglycerin sublingual, and morphine at 0.1 mg/kg.

C.   Place patient on a monitor, establish IV access, and administer CPR while preparing a cardiac defibrillator.

D.   Place patient on a monitor, establish IV access, and administer adenosine 6 mg rapid IV push.

E.   Place patient on a monitor, establish IV access, and administer a one liter fluid bolus of normal saline

___
2. Electrical capture by transcutaneous pacing is confirmed by which of the following?

A.   A p-wave, QRS complex, and t-wave showing a first-degree heart block pattern

B.   A pacing spike followed by a p-wave, QRS complex, and t wave all of normal morphology

C.   A return to normal rate with no change in rhythm

D.   A return to normal sinus rhythm with normal rate

E.   A widened QRS after each pacing spike

___

3. Which of the following statements regarding cardiac pacing is true?

A.   Although alternative approaches are acceptable, the femoral vein is the preferred site of percutaneous access for placement of the transvenous pacer.

B.  Hypothermia is a relative contraindication to transvenous pacing.

C.  Second degree heart block type I (Wenckebach)  is among the indications for transvenous pacing.

D.  Transvenous pacing is underutilized in traumatic cardiac arrest and evidence suggests that it may be beneficial in some cases

E.  When compared with the blind insertion technique, ECG-guided transvenous pacer insertion has been shown to be faster.

Discussion

A 75-year-old female presented to the emergency department with hypotention and bradycardia.  ACLS guidelines for symptomatic bradycardia were initiated including IV fluid resuscitation, administration of repeat doses of atropine 0.5mg IVP and placement of transcutaneous pacer.  Her HR remained below 60 bpm with these interventions and therefore transcutaneous pacing was initiated.  Her condition was refractory to transcutaneous pacing as well and so a transvenous pacer was placed.

The right internal jugular was chosen as the site to place the transvenous pacer.  The patient was draped in a sterile fashion and ultrasound guidance was used to obtain percutaneous access of the right internal jugular vein.  After inserting of the transvenous pacing catheter the catheter balloon was inflated and the catheter was floated down the internal jugular vein with ECG-guidance to the superior vena cava, into the right atrium.  Pacing was confirmed by an ECG pattern of an electrical spike followed by a wide QRS complex (see illustration below). After placement of this pacer, the heart was paced at a rate of 60 bpm.  Check out this review article on transcutaneous pacing.

pic

When a patient presents with bradycardia one must first determine if emergent intervention is warranted.  A small percentage of the population has a physiological heart rate of less than 60 bpm.  This patient, in contrast, was having generalized weakness and decreased responsiveness and therefore symptomatic bradycardia.  According to ACLS guidelines, hypotension is one of the “signs or symptoms of poor perfusion caused by the bradycardia.”  Atropine administration, transcutaneous pacing, and later transvenous pacing were all employed to stabilize this patient.  She eventually achieved stability with transcutaneous pacing.

These interventions were administered emergently before any laboratory results had returned.  Laboratory results indicated that electrolyte imbalances and dehydration were contributing factors.  The patient was admitted to the MICU and was eventually discharged after correction of her electrolyte abnormalities and dehydration.

When one is presented with a medical code situation in the emergency department whose conditions fit the criteria for one of the ACLS algorithms, the steps for the appropriate algorithm must be followed emergently.  The underlying cause will often not be apparent at initial presentation to the emergency department.  And once it is discovered it must be addressed.

ANSWERS

1.  The correct answer is A, “Place patient on a monitor, establish IV access, and administer 0.5 mg doses of atropine while preparing for transcutaneous pacing.”  The patient’s ECG shows a junctional bradycardia.  Proper treatment of this patient requires following ACLS guidelines for symptomatic bradycardia.  Current ACLS guidelines for intervention in bradycardia are for patients who have “signs or symptoms of poor perfusion caused by the bradycardia.”  Treatment includes administration of atropine 0.5 mg IV while preparing for transcutaneous pacing.  Atropine may be repeated to a total of 3 mg, otherwise the patient is at risk for anticholinergic toxicity.  Epinephrine and dopamine may also be considered.  If the patient’s condition is refractory to medical management, transcutaneous pacing, followed by  transvenous pacing may be indicated.

(B) is incorrect because it specifies the proper treatment indicated in the ACLS algorithm for acute coronary syndrome, not for symptomatic bradycardia.  Although ACS may be on this patient’s initial list of differential diagnoses, her condition should be treated immediately as symptomatic bradycardia.  If during the course of treatment the patient’s clinical picture begins to exhibit signs or symptoms more specific to ACS, then this patient may need to be treated with aspirin, nitroglycerine, and morphine.

(C) is incorrect because this patient has palpable pulses and CPR is only indicated in patients who are pulseless.  Asynchronous cardioversion is indicated only in pulseless patients and synchronized cardioversion is indicated in certain cases of tachycardia with pulses.  Neither form of cardioversion is indicated in bradycardia.

Administration of adenosine is indicated in the stable patient who is suspected to have a supraventricular tachycardia (AVnRT and AVRT). Answer choice (D), therefore, is incorrect.

Although a fluid bolus is often indicated in hypotension, it is not part of the symptomatic bradycardia treatment algorithm and therefore (E) is incorrect.  This patient’s hypotension may be thought of as a clinical sign of “poor perfusion caused by the bradycardia”  And improving the bradycardia will likely result in an improved blood pressure.  Nonetheless, fluids should be started to augment the patient’s blood pressure.

2.  The correct answer is E, “A widened QRS after each pacing spike.”  Under physiologic conditions, the ventricles of the heart are depolarized rapidly by the rapid progression of an electrical current through the His-Purkinje system, causing the QRS complex to take on a narrow appearance.  When the heart is paced from an external pacing source, such as and artificial pacer, ventricular depolarization takes more time, causing the QRS complex to take on a wide appearance.  The initiation of the electrical impulse by the pacemaker itself can be seen on the ECG as a very narrow spike.

An electrical impulse that begins at the SA node and progresses down all of the heart’s physiological pathways would be required to produce a P-wave, QRS complex, and T-wave of normal morphology, or to produce a pattern consistent with first-degree heart block.  Transcutaneous cardiac pacing does not begin at the SA node and does not progress in this manner.  Answer choices A and B, therefore, are incorrect.

Transcutaneous pacing therapeutically changes the cardiac rate and it also changes the rhythm so that the ECG shows pacing spikes followed by wide QRS complexes when capture is achieved.  Therefore C and D are both incorrect answers.

3.  The correct answer is: B, “Hypothermia is a relative contraindication to transvenous pacing.”  Introducing a transvenous pacer into a patient who is hypothermic has a theoretical potential of causing the patient to have a terminal dysrhythmia.  Hypothermia, therefore, is considered a relative contraindication to transvenous pacing.  Hypothermic patients should be warmed according to standard hypothermic care.

When placing a transcutaneous pacer, either the right internal jugular vein or the left subclavian vein should be considered first as they have been shown to have “the highest rates of proper placement in code situations” (Harrigan et al).  Answer choice A, therefore, is incorrect.  The femoral approach may be indicated in the coagulopathic patient.

Although electronic cardiac pacing may be considered in advanced forms of AV nodal block, second degree heart block type I (Wenckebach) is relatively benign and an invasive procedural is generally not warranted.  Answer choice C, therefore, is incorrect.

Answer choice D is incorrect because cardiac pacing is not indicated in traumatic cardiac arrest.

Although there are advantages to the ECG-guided technique for transvenous pacer insertion, speed is not one of them.  The blind technique is, in fact, faster, making answer choice E incorrect.

References
Harrigan RA, Chan TC, Moonblatt S, Vilke GM, Ufberg JW. Temporary Transvenous pacemaker placement in the emergency department. J Emerg Med 2007;32: 105-11.

This case discussion presented by Jeff McMenomy, MD.

Intern Report Case 1.2

intern-report

History of Present Illness:
A 75-year-old woman is brought to the Emergency Department by EMS. Her family states the patient complained of gradually worsening generalized weakness and decreased responsiveness over the course of the previous week.  They also state that she is “not being herself”.  EMS noted the patient to be minimally responsive, bradycardic, and hypotensive en route to the hospital.

PMHx: hypertension
PSHx: unknown
FHx: unknown
SocHx: unknown
Allergies: codeine, penicillin
Medications: unknown

Physical Exam

Vitals: T 36.2 C, HR 40, BP 86/43, RR 18, O2 97% on 15 L nonrebreather
Gen: obtunded, oriented x 1, responds to name but not oriented to place or time
HEENT: NC/AT, PERRL, EOMI, no conjunctival pallor, TMs clear b/l, mucous membranes dry, no tonsillar exudates or erythema, + gag reflex
Neck: supple, FROM, no JVD, trachea midline, no cervical LAN
Heart: bradycardic, regular rhythm, no murmurs, rubs, or gallops.
Lungs: clear to auscultation b/l in all fields, no wheezes/rales/rhonchi, normal respiratory effort
Abdomen: soft, nontender, nondistended, bowel sounds normoactive, no rebound/masses/guarding
Vascular: capillary refill 3 seconds, pulses thready but palpable in all four extremities.
Neuro: responds to her name, follows commands. Eyes open spontaneously.  Tongue and uvula are midline.  Moving all four extremities.
Skin: + mild diaphoresis, no rashes

Electrocardiogram:

ecg1

QUESTIONS:

1. Given this patient’s overall clinical picture, what would be the most appropriate initial course of action?

A.   Place patient on a monitor, establish IV access, and administer 0.5 mg doses of atropine while preparing for transcutaneous pacing.

B.   Place patient on a monitor, establish IV access, and administer 325 mg of aspirin, 0.4 mg nitroglycerin sublingual, and morphine at 0.1 mg/kg.

C.   Place patient on a monitor, establish IV access, and administer CPR while preparing a cardiac defibrillator.

D.   Place patient on a monitor, establish IV access, and administer adenosine 6 mg rapid IV push.

E.   Place patient on a monitor, establish IV access, and administer a one liter fluid bolus of normal saline

___
2. Electrical capture by transcutaneous pacing is confirmed by which of the following?

A.   A p-wave, QRS complex, and t-wave showing a first-degree heart block pattern

B.   A pacing spike followed by a p-wave, QRS complex, and t wave all of normal morphology

C.   A return to normal rate with no change in rhythm

D.   A return to normal sinus rhythm with normal rate

E.   A widened QRS after each pacing spike

___

3. Which of the following statements regarding cardiac pacing is true?

A.   Although alternative approaches are acceptable, the femoral vein is the preferred site of percutaneous access for placement of the transvenous pacer.

B.  Hypothermia is a relative contraindication to transvenous pacing.

C.  Second degree heart block type I (Wenckebach)  is among the indications for transvenous pacing.

D.  Transvenous pacing is underutilized in traumatic cardiac arrest and evidence suggests that it may be beneficial in some cases

E.  When compared with the blind insertion technique, ECG-guided transvenous pacer insertion has been shown to be faster.

___

Please submit your answers to the questions in the “leave a reply” box or click on the “comments” link.  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.