Case Presentation by Dr. Meena Munshi

CHIEF COMPLAINT: “I feel short of breath.”

HISTORY OF PRESENT ILLNESS:

21-yo F with sickle cell anemia is brought into resuscitation from walk-in triage for tachycardia (HR 150s) with multiple complaints including: shortness of breath, dizzy/lightheadedness, cough with bright red blood-tinged sputum, and “bloody pee”

Shortness of breath occurs at rest and with exertion, without positional component. Has a slight cough with a few drops of blood tinged sputum. Was admitted to the hospital 10 days ago with community acquired pneumonia and acute chest syndrome, given IV antibiotics, an exchange transfusion, and discharged home 4 days ago with doxycycline of which she completed a 7 day course today. Shortness of breath began when she was diagnosed with CAP but improved during hospital stay and with home antibiotics until today when it suddenly got worse. Denies chest pain, wheezing, sick contacts, history of PE, leg swelling, or asthma.

Feels fatigued and lightheaded at rest, with exertional exacerbation. No fever, syncope, weight loss, headache, neck pain, palpitations, diaphoresis, room-spinning sensation, abdominal pain/distention, nausea or vomiting. Loose brown stools today, without melena or hematochezia.

Notes worsening yellowing of her skin related to sickle cell anemia. No petechiae, bruising, pruritis.

What really brought her in was that for the last few hours, she has been “peeing out blood.” States this is not blood-tinged urine but frank blood. Denies previous such occurrence or any suprapubic or flank pain, dysuria, polyuria, urgency, frequency, vaginal bleeding, or menstruation.

PERTINENT REVIEW OF SYSTEMS:

GENERAL: Generalized weakness, chills and fatigue; no fever or night sweats

HEAD:  Lightheadedness, without syncope or headache.

EAR, NOSE AND THROAT:  No bleeding gums.

CARDIAC: No chest pain, palpitations, orthopnea, PND or leg swelling.

RESPIRATORY:  Shortness of breath and hemoptysis

GI:  No abdo pain, N/V, melena, hematochezia, hemetemesis. Loose stools.

GU:  Gross hematuria, but no dysuria, urgency, frequency, vaginal bleeding

MUSCULOSKELETAL:  No myalgias, arthralgias, joint swelling

ENDOCRINE:  No heat/cold intolerance, polyuria or polydipsia.

SKIN:  Yellowing of eyes and skin, but no bruising, rashes, or pruritis

PMH:  Sickle cell anemia (HbSS), recent CAP with acute chest syndrome requiring plasma exchange transfusion and pRBCs. Multiple (4-5) prior blood transfusions for SCA.

PSH:  Cholecystectomy, left eye muscle repair.

Meds:  Tylenol with Codeine, Motrin.

ALLERGIES:  NKDA

FH:  DM, HTN, and Sickle cell trait. No DVT/PE, cancer or CAD

SH:  Denies use of alcohol, tobacco, or drugs.

LMP: Cannot recall; periods are irregular. Not sexually active.

EXAMINATION OF ORGAN SYSTEMS-BODY AREAS:

VITALS:  BP 104/76, HR 152, RR 24, oral T 37.7, pulse ox 97% RA

GENERAL:  Obese female appears tired and jaundiced, but in no acute distress.

PSYCH:  Alert and oriented x4, cooperative.

HEENT:  NCAT, PERRLA (4 mm b/l), profound conjunctival pallor and scleral icterus.  No epistaxis/rhinorrhea.  Pale,  moist oral mucosa. No oropharyngeal erythema, exudates or lesions.  No cyanosis.

NECK:  Supple, no JVD, lymphadenopathy or meningismus.  Trachea is midline.

PULMONARY:  Tachypnea(30s). CTA b/l without wheeze/rales/ronchi/stidor or use of accessory muscles. Speaks in complete sentences.

CARDIOVASCULAR:  Tachycardia (140s to 150s). No murmurs/gallops/rubs/S3/S4.

ABDOMEN:  Soft, nontender, nondistended, normal BS. No hepatosplenomegaly. No guarding, rigidity or rebound tenderness.  FOBT negative.

MUSCULOSKELETAL:  Back and extremities, atraumatic, nontender with FROM. No peripheral edema, calf tenderness or asymmetry. Extremities well perfused.

NEURO:  EOMI.  Normal speech and hearing.  Face is symmetric.  Moving all extremities with good and symmetric motor strength. Sensation grossly intact. Gait not assessed.  GCS 15. Normal mental status.

SKIN:  Pallor with yellow-orange skin discoloration.  Scleral icterus.  No petechiae, contusions, hematomas or ther acute rashes or lesions.

LABS:

CBC: today                vs     baseline   

H/H 4.7/14.5              vs        8/24

WBC 30                         vs      10-17

Plt 825,000                  vs      750,000

Reticulocyte 12%         vs      25%

Retic count 186,700   vs      500,000

Urinalysis:

turbid brown

urine bilirubin 3+

blood 3+

urine protein 3+

urobilinogen 4+

RBCs 2-5

WBCa 2-5

CMP:

Na                   136

K                    3.6

Cl                  101

CO2                19

BUN              29

Cr                  1.2 (baseline 0.6)

Gluc            115

T. Bilirubin      4.5 (0-1.5)

D. Bilirubin      1.7 (0-0.4)

AST                  23

ALT                  30

Alk Phos            109

Troponin: negative

Serum preg test: negative

Type and Cross: 2U pRBCs; Blood type B+

Direct Antigen Test: positive

LDH: 1476 (nml 100-240)

EKG: Sinus tachycardia (HR 152)

QUESTIONS:

1)  The patient’s symptoms are most likely due to:

a) Aplastic crisis

b)  Delayed hemolytic transfusion reaction

c)  Splenic sequestration

d)  Vaso-occulsive sickle cell pain crisis

e)  Anxiety

2)  The patient was normotensive and afebrile throughout her ED stay. Her tachycardia improved (150s–> 110s) with bolus NS hydration. Tachypnea and shortness of breath improved with 2L oxygen via nasal cannula. She remains alert otherwise well. After reevaluating the scenario, you decide to:

a)  Continue supportive treatment, observe, hold off on transfusion

b)  Transfuse 2U pRBCs

c)  Transfuse 1U pRBCs

d)  Transfuse whole blood

e)  Discharge home with close Hematology follow up

3)  In this patient which condition(s) would warrant a blood transfusion?

a)  A typical pain crisis

b)  Drop in hemoglobin 2 units below baseline with symptomatic anemia

c)  Pregnancy

d)  Stroke

e)  Chest pain with cough, fever, purulent sputum

Case Presentation by Dr. Katie Ohlendorf

Chief Complaint:

Possible stroke.

History of Present Illness:

The patient is a 78 year old female with no prior CVA.  The patient was last seen well by her son yesterday evening.  Today, the patient was supposed to go to her grandson’s birthday party.  She did not show up and her son has been trying to call the patient for the prior 3 hours without response.  EMS was called to the patients home.  Here, she was found with slurred speech, left sided gaze and left sided hemiparesis.

The patient is following commands.  She is difficult to understand secondary to severe dysarthria.  She denies dyspnea or chest pain.  She cannot tell us when her neurological symptoms started.

Review of Systems:

Per HPI – unable to obtain further secondary to patients severe dysarthria.

Past Medical History:

Hypertension, palpitations, rheumatic fever, pneumonia, and breast cancer.

Past Surgical History:

Lumpectomy, hysterectomy, cardiac ablation, and cardiac valve replacement.

Medications:

Coumadin, multivitamins, metoprolol, docusate, vitamin D3, calcium carbonate, Arimidex, and alendronate.

Allergies:

Penicillin.

Family History:

Not obtained. 

Social History:

Negative for alcohol and smoking.  The patient presents with her son.

Examination of Organ Systems and Body Areas:

VITAL SIGNS:  Blood pressure 184/80, pulse 101, respirations 18, temperature 37.5 temporal, and pulse ox on room air 99%.

GENERAL:  The patient is awake and alert.  Does not appear to be in acute cardiopulmonary distress.

HEENT:  Pupils equal, round andreactive, although gazing to the right.  No conjunctival injection or subconjunctival hemorrhage.  Unable to assess her hearing.  No hemotympanum.  Droop to her left face.  No pus or redness in the posterior pharynx.  Intact gag reflex.

NECK:  Supple without adenopathy.

RESPIRATORY:  Symmetrical breath sounds.  No rales, rhonchi or wheezes.

CARDIAC:  Regular rate and rhythm without murmur, rub or gallop.  Patient has a valvular click from prosthetic aortic valve.

GASTROINTESTINAL:  Soft, nontender.  Active bowel sounds.  No organomegaly, hernias or masses.  Bowel sounds present in all quadrants.

MUSCULOSKELETAL:  Hemipareses, left side.

NEUROLOGIC:  Patient awake and alert.  Dysarthric speech. Hearing unable to be assessed.  Right sided gaze preference.  Left sided facial droop.  Intact gag reflex.  Left sided hemiparesis with 0/5 muscle strength with left upper and left lower extremity.  5/5 muscle strength with right upper and right lower extremity. Receptive wise, she processes her questions fairly well.

SKIN:  No rash.

Labs:

Na:  139

K:  4.3

Cl:  100

HCO3:  11

Glucose:  139

BUN:  11

Cr:  0.8

Ca:  9.3

Troponin:  <0.017

WBC:  16.7

Hb:  17.1

Hct:  47.2

Plts:  224

PTT:  40.8

PT:  43.7

INR:  4.14

Imaging:

Questions:

1) How would you manage a warfarin induced coagulopathy if…

1. a.     The INR is between 3.5 to 5 without significant bleeding
2. b.    The INR is between 5-9 without significant bleeding
3. c.     The INR is > 9 without significant bleeding
4. d.    The patient has an elevated INR and life threatening bleeding

2) How do you manage a heparin induced coagulopathy in a patient with…

1. e.     Minor bleeding
2. f.      Major bleeding

3) How do you manage a patient on Pradaxa with significant bleeding?

Answer Choices:

I.  Administer 10 mg of vitamin K with a slow IV push and 10 – 15 ml/kg of FFP

II.  Hold next 1 – 2 doses and consider oral vitamin K 1 – 2.5 mg

III. Consider hemodialysis, PCC and rFVIIa

IV.  Stop heparin administration

V. Hold next 1 – 2 doses and administer oral vitamin K 2.5 – 5 mg

VI.  Lower or admit next dose of warfarin

VII.  Protamine 1 mg per 100 units of total amount of IV heparin administered within the past 3 hours

Answers:

1) a.  VI.

     b.  II.

     c.  V.

     d.  I.

2) a.  IV.

     b.  VII.

3) III.

Discussion:

There are several anticoagulants on the market today.  Anticoagulants are used in the management of many conditions – they may stop further thrombosis reduce the risk of a thromboembolic event, or help prevent thrombi from forming.  One of the biggest risks of using these agents is hemorrhage and life threatening bleeding.  We will discuss the pharmacology and the complications and management of the various anticoagulants available today.

Warfarin (Coumadin)

Warfarin is the most common oral anticoagulant encountered in the emergency department.  It works by blocking the activation of vitamin K and therefore interferes with the vitamin K dependent clotting factors II, VII, IX and X.  This provides the antithrombotic effect via the extrinsic coagulation pathway (“The EX patriot went to WARfarin”).  Warfarin also has a pro-thrombotic effect via inhibition of proteins C and S.  During maintenance therapy, the antithrombotic effect outweighs the pro-thrombotic effect.

The pro-thrombotic effect is greatest when starting and discontinuing warfarin therapy.  Therefore, when starting warfarin therapy it is necessary to bridge with a parental anticoagulant (such as heparin) until the international normalized ratio (INR) reaches the therapeutic range.  It is also necessary to gradually taper warfarin when discontinuing this medication.  This is due to the differences in the half-lives of the clotting factors and proteins C and S.  The clotting factor half-lives vary from 7 hours (factor VII) to 60 hours (factor II), whereas the antithrombotic proteins have shorter half-lives of 8 hours.

Dosing of warfarin is guided by measuring the INR.  Normal therapeutic range is 2-3.  The INR of 2.5 to 3.5 is goal for those with mechanical heart valves and those who have antiphospholipid antibody syndrome.  The risk of bleeding increases with the increasing INR.

To manage a warfarin coagulopathy you must consider the INR, the patient status, and whether or not they have significant bleeding.  To reverse a warfarin coagulopathy the first step is to hold warfarin, the next to administer vitamin K, and the final is to administer fresh frozen plasma (FFP), prothrombin complex concentrate (PCC) or recombinant Factor VIIa (rFVIIa).

For asymptomatic patients the first step is to hold the next dose to two doses of warfarin.  If the patient is at a high risk of bleeding with an INR of 5-9, consider PO vitamin K administration.  If the INR is > 9 and no significant bleeding then administer 2.5 to 5 mg of PO vitamin K.

Oral vitamin K will decrease the INR in approximately 16 hours (longer if INR > 10).  Oral vitamin K will decrease the INR faster than subcutaneous vitamin K if the INR is < 10.  IV vitamin K may also be used.  This is associated with risk of anaphylaxis and is not used in the routine reversal of anticoagulation.  IV vitamin K also carries a risk of over correction and is reserved for those with life threatening bleeds or those who ingested a rodenticide.  The peak effect from vitamin K is seen in 1-2 days.

FFP is used if there is life threatening bleeding present.  It is the fastest way to reverse the anticoagulant effects of warfarin, and is considered safe.  Administer FFP at a dose of 10-15 mL/kg (typically 3-4 units).

Rapid (and complete) reversal of warfarin may be achieved by PCC or rFVIIa.  PCC contains factors II, VII, IX and X and works in under 30 minutes.  The dose is 25-50 units/kg.  rFVIIa dose is 5 mcg/kg (typical dose is one 1200 mcg vial).  May repeat the dose if INR remains elevated.

Heparin and Low Molecular Weight Heparin

Unfractionated heparin (UFH) activates antithrombin III (AT III), leading to the inhibition of Factor Xa and thrombin.   Heparin has a very short half life (30-150 minutes) and must be given arenterally.  It has a relatively unpredictable anticoagulation effect and requires frequent monitoring of the activated partial thromboplastin time (aPTT).  Goals with therapy are usually an aPTT 1.5 to 2.5 times the normal range.  Heparin may affect the PT and INR, but this is not used to guide therapy.

If bleeding develops while a patient is on UFH, you must first stop the heparin administration.  The aPTT may lag behind the actual anticoagulation dosing; therefore you cannot rely on the aPTT to predict whether your patient has a serious bleed.

Protamine is used to reverse UFH in severe bleeding.  One milligram IV protamine neutralizes 100 units of UFH administered in the prior 3 hours.  Protamine has a risk of anaphylaxis.  It should be given slowly over 1 to 3 minutes and not exceed 50 mg in a 10 minute period.  Protamine has a very short half life (7 minutes) therefore may require more than one dose.

Low molecular weight heparin (LMWH) also work by binding  AT III and deactivation of Factor Xa.  LMWH’s include enoxaparin (Lovenox), dilteparin and tinzaparin.  The half life is longer than UFH and therefore allows for once or twice a day dosing.

LMWH usually cause less bleeding than UFH.  Protamine will not completely reverse the anticoagulant effect of LMWH, only reversing 60% of function.  rFVIIa has been reported to stop severe bleeding with use of LMWH.

Fondaparinux  (Arixtra)is a synthetic drug that is a selective Factor Xa inhibitor.  The use of protamine does NOT reverse fondaparinux.  Hemodialysis (HD) will reduce the level by 20%.  rFVIIa may be used to reverse serious bleeds.

Dibigatran (Pradaxa)

Dibigatran is a competitive, direct thrombin inhibitor.  This prevents development of a thrombus via direct clotting factor inhibition (not depletion).  It is approved for use in atrial fibrillation to help prevent thromboembolism.

Laboratory testing may help determine if dibigatran is contributing to the bleeding event.  aPTT is insensitive to the effects of dibigatran.  If the aPTT is normal this suggests little anticoagulant activity present, but even mild elevations in aPTT can be associated with significant bleeding.  Thrombin time (TT) is less helpful in overdose, but a normal TT excludes the presence of significant dibigatran levels.  Ecarin clotting time (ECT) has a linear relationship with dibigatran levels, although this test is not available at all facilities.

There is no reversal agent for dibigatran.  In an acute overdose, activated charcoal may help in absorbing dibigatran.  Because dibigatran is a direct thrombin inhibitor, administration of clotting factors (FFP, PCC) is unlikely to be helpful in reversal of coagulation.  They may be administered only as a last resort when supportive measures fail to control the bleed.  If a patient develops life threatening bleeding while on dibigratan, consider hemodialysis (primarily excreted in urine, HD will remove approximately 60% of the drug) and the use of rFVIIa and PCC.

http://healthcare.utah.edu/thrombosis/newagents/TS.Dabi_Bleeding.pdf

http://emcrit.org/misc/bleeding-patients-on-dabigatran/

Rivaroxaban (Xarelto)

Rivaroxaban is a direct Factor Xa inhibitor.  It is approved for the prevention of stroke and thromboembolism in patients with atrial fibrillation and prevention of thrombus in those who are undergoing knee or hip replacement surgery.

Laboratory testing will show a dose dependent effect on PT and aPTT, however this is not a reliable test.  Similarly the INR is not sensitive to the effects of rivaroxaban.  There are new laboratory testing under development to help determine the level of anticoagulation achieved with rivaroxaban.

There are no reversal agents available.  If a patient has minor bleeding either discontinue therapy or delay the next dose.  If there is moderate to severe bleeding, initiate supportive treatment (blood, IVF, cardiac monitoring)and try to control the site of the bleeding.  Oral charcoal may be administered if rivaroxaban was administered within the prior 2 hours.  Unlike dibigatran, rivaroxaban is NOT dialyzable.  If severe/life threatening bleeding PCC may be tried.

Great resource on anticoagulant reversal:

http://kpssctoxicology.org/pdf/Anticoagulant%20reversal_.pdf

Case Presentation by Dr. Dan Seitz

A middle aged African-American John Doe, presents as a medical code. On arrival the patient is actively seizing. According to EMS the patient has been seizing for approximately 40 minutes prehospital. After eight rounds of lorazepam pushes the patient continues to have seizure activity. The decision is made to load the patient with one gram of phenytoin, start a lorazepam drip and intubate the patient. Rapid sequence intubation is performed using etomidate and succinylcholine. For post-intubation sedation and to facilitate imaging studies the patient receives morphine, the lorazepam drip and gets two doses of vecuronium while in the ED. The patient is transferred to the Neuro ICU for further management.

Questions:

1)  The patient receives a considerable amount of both lorazepam and phenytoin. What solvent must you be aware of which can cause hyperosmolarity and metabolic acidosis?
a) Ethylene glycol
b) Fluoxetine hydrochloride
c) Levamisole
d) Propylene glycol

2)  The patient is found to be severely hyperkalemic. Which medication likely worsened this?
a) Etomindate
b) Lorazepam
c) Phenytoin
d) Succinylcholine

3)  What is the most common complication of multiple doses of paralytics?
a) Hyperkalemia
b) Paresthesias and peripheral neuropathies
c) Prolonged paralysis and myopathy
d) Rhabdomyolysis

4)  In the ICU the patient is found to be septic. He develops hypotension that is refractory to IV fluids and pressors. Administration of which medication should be considered?
a) Hydrocortisone
b) Neostigmine
c) None – permissive hypotension is appropriate in this setting
d) Xigris (activated protein C)

BONUS QUESTION:
5)  After administering a paralytic agent – the patients eyes will be:
a) Reactive to light
b) Non-reactive to light

Answers:

1) D   2) D   3) C   4) A   5) reactive

An awareness of the potential adverse effects of medications that we order is essential in becoming a competent physician.  We often administer medications in the Emergency Department and these adverse effects do not materialize until the patient reaches the floor or the ICU.  This case highlights just a few of these potential adverse effects.

1)  D.   In some instances adverse effects are the result of a medication additive.  Propylene glycol is the primary solvent in lorazepam, phenytoin, etomidate and some “environmentally safe” antifreeze preparations.   Propylene glycol is a clear, odorless, colorless viscous liquid – which is hepatically metabolized to lactic acid.  Adverse effects of large volumes of propylene glycol include cardiovascular toxicity (hypotension, bradycardia and QRS widening), neurotoxicity (seizures – in particularly in small infants), and electrolyte/metabolic disturbances (hyperosmolality and lactic acidosis).  Alternatives to these agents include midazolam, phosphenytoin and ketamine – which do not contain propylene glycol.

2)  D.  The most important adverse effect of Succinylcholine is its potential to induce hyperkalemia.  Which has been lethal and life threatening in many case reports.  Succinylcholine will typically cause a 0.5 mEq/L elevation in a patient’s potassium.  This only become clinically significant in patients who present with diseases that cause ACh regulator upregulation:

• Denervating injuries or diseases (eg, stroke, spinal cord injury, MS, ALS
• Inherited myopathies (eg, muscular dystrophy)
• Burns – subacute
• Crush injuries
• Rhabdomyolysis or risk of rhabdomyolysis

3)  C.  The most important thing to remember when redosing paralytics is that they have no analgesic or amnestic properties.  Never give paralytics as monotherapy.  The most common side effect of multi-dose paralytics is myopathy and prolonged paralysis.  This “critical illness polyneuromyopathy” is associated with prolonged ventilation and worse outcomes.  As with all medication weight the pros and cons (risk of self extubation – is never a good thing), and act in the best interest of your patients.

4)  A.  There is a long standing debate regarding the usage of etomidate as an induction agent.  Proponents of drug argue that in these septic patients you should not risk immediate hemodynamic stability (etomidate does not worsen hypotension), that cortisol levels do not fall below physiological levels, and that in prospective randomized controlled trials there has been no differences shown in mortality.  Opponents of the drug argue that etomidate inhibits cortisol synthesis, depressing cortisol levels for 12-24 hours; this is logically not beneficial for sick patients who are attempting to mount a stress response.  Opponents also argue that while mortality may be the same, morbidity is not.  Single dose Etomidate has been shown to increase ICU stays, duration of intubation and hospital length of stays.  Whatever side of the fence that you may fall on; in our clinical scenario consideration should be made for the possibility of adrenal suppression and 100 mg of hydrocortisone should be administered.

As an aside Xigris is officially dead.

BONUS QUESTION:
Pupillary light reflex is NOT altered by neuromuscular blocking drugs.  As shown in Archives of Neurology in 1997, and re-proven in Annals of EM – March, 2011.  The second article has lots of discussion on the Annals Journal Club website.  Read the articles and see for yourself the next time that you intubate a patient.

REFERENCES

Manual of Toxicologic Emergencies.  Goldfrank.

Samantha Wood, Michael E. Winters, Care of the Intubated Emergency Department Patient, The Journal of Emergency Medicine, Volume 40, Issue 4, April 2011, Pages 419-427, ISSN 0736-4679, 10.1016/j.jemermed.2010.02.021.

The effect of etomidate on adrenal function in critical illness: a systematic review.  Albert SG, Ariyan S, Rather A.  Intensive Care Med. 2011 Jun;37(6):901-10. Epub 2011 Mar 4

Gray AT, Krejci ST, Larson MD. Neuromuscular blocking drugs do not alter the pupillary light reflex of anesthetized humans. Arch Neurol. 1997;54(5):579-584.

David A. Caro, Steven Andescavage, Mohsen Akhlaghi, Colleen Kalynych, Robert L. Wears, Pupillary Response to Light Is Preserved in the Majority of Patients Undergoing Rapid Sequence Intubation, Annals of Emergency Medicine, Volume 57, Issue 3, March 2011, Pages 234-237, ISSN 0196-0644, 10.1016/j.annemergmed.2010.10.017.

Case Presentation by Dr. Matt Steimle

You are starting your shift at a small rural hospital with limited resources.

At the start of your shift during transition of care, you receive sign out about a 63-year-old male who has chest pain, is undergoing a cardiac workup, and is admitted to his own internal medicine doctor with a cardiology consult. You are told his first EKG has first-degree atrioventricular block unchanged from prior EKGs and that his first troponin I is negative. He has received aspirin and a dose of nitroglycerin.

His vital signs at the time of transition of care: BP 145/94, P 65, R 20, T 37.1, and 100% saturation on 2L O₂ by nasal cannula

His repeat EKG and troponin I are ordered to be drawn in 3 hours.

2 hours into your shift you notice that the patient is lightheaded and confused, and the family and the nursing staff indicate that this is a sudden change. You examine him and order another 12-lead EKG.

Pertinent findings on repeat physical exam:

Vitals: BP 70/40, P 39, R 20, T 37.2, 100% saturation on 2L O₂ by nasal cannula

General: complains of feeling presycopal and lightheaded

Cardiac: bradycardic, no M/R/G, s1 and s2 normal

Neuro: a+ox3, but is slow to respond; otherwise the rest of your neuro exam is unremarakable

Questions:

1. Which venous site is preferred for transvenous pacemaker placement?
a) brachial
b) left internal jugular
c) right internal jugular
d) right subclavian

2. What should the initial settings be on the pulse generator?
a) rate 60 beats/min or 10 beats faster than the underlying ventricular rhythm, output 5 mA, sensitivity 10 mV
b) rate 70 beats/min or 10 beats faster than the underlying ventricular rhythm, output 5 mA, sensitivity 10 mV
c) rate 80 beats/min or 10 beats faster than the underlying ventricular rhythm, output 5 mA, sensitivity 10 mV
d) rate 80 beats/min or 10 beats faster than the underlying ventricular rhythm, output 5 mA, sensitivity 3 mV

3. Which EKG lead do you connect the pacemaker to?a) II

b) III
c) AVL
d) V1

4. When do you inflate the balloon?
a) 10-12 cm for a subclavian or internal jugular insertion
b) 14-16 cm for a subclavian or internal jugular insertion
c) 16-18 cm for a subclavian or internal jugular insertion
d) 8-10 cm for a subclavian or internal jugular insertion

5. What will the EKG show when the pacemaker is in the right ventricle?
a) both the P-wave and QRS complex will be negative
b) P-wave becomes large and biphasic
c) P-wave becomes smaller and the QRS complex becomes larger
d) P-wave is larger than the QRS complex and deeply inverted

6. When the sensitivity control is in the demand (synchronous) mode, the pacemaker does not sense ventricular depolarizations.

a) False

b) True

Answers:

1. c

2. d

3. d

4. a

5. c

6. a

Discussion:

Heart block is a known complication of acute myocardial infarction (AMI).  15% to 19% of AMI patients progress to some degree of heart block. First-degree atrioventricular (AV) block progresses to second- or third-degree AV block 33% of the time, and second-degree AV block progresses to third-degree AV block about 33% of the time.

AV block occurring during anterior wall AMI is believed to occur due to diffuse ischemia of the septum and infranodal conduction tissue. These patients can progress to higher-degree AV block without warning, and consideration should be given to “prophylactic” cardiac pacemaker placement in such patients. Hemodynamically unstable patients unresponsive to medical therapy should be paced. One should try transcutaneous cardiac pacing until a transvenous pacemaker can be placed.

Temporary cardiac pacing for bradyarrhythmias in acute myocardial infarction may be necessary, even though permanent cardiac pacing may not be required. Revascularization strategies with thrombolysis and angioplasty have reduced the need for permanent pacing since there is less myocardial damage and a greater chance that bradycardia and conduction abnormalities will resolve. Therefore, there may be a need for temporary cardiac pacing.

An important consideration in the setting of AMI is that bradycardia, even if asymptomatic or transient, can cause decreased coronary blood flow and reduced myocardial perfusion.

Guidelines from the American Heart Association and American College of Cardiology recommend temporary cardiac pacing in patients with AMI and the following cardiac rhythms and conduction abnormalities:

1.            Asystole

2.            Symptomatic bradycardia due to sinus node dysfunction, or Mobitz type I             (Wenckebach) second degree AV block that is not responsive to atropine therapy

3.            Mobitz type II second degree or complete heart block

4.            Bilateral or alternating bundle branch block, including right bundle branch block             with left anterior fascicular block or left posterior fascicular block

5.            A new bundle branch block with either old or new first degree AV block

6.            An old right bundle branch block with first degree AV block and a new fascicular             block

There are complications with the insertion of a endocardial pacemaker in a patient who has received thrombolytic therapy and is being treated with aggressive anticoagulant and antiplatelet therapy. In these settings, transcutaneous pacing is preferred. Insert endocardial pacemaker only if warranted due to recurrence of symptoms.

Avoid temporary pacing:

1. When the risks outweigh the benefits

2. When there are intermittent, mild or rare symptoms, and the bradycardia is well tolerated. This includes mildly symptomatic (mild or rare symptoms) complete heart block with an adequate and “stable” escape rhythm or symptomatic sick sinus syndrome with only rare pauses

3. In the presence of a prosthetic tricuspid valve or right ventricle infarct (remember to obtain right-sided leads RV3 and RV4), a circumstance in which it may not be possible to achieve right ventricle capture

4. In a patient with AMI who has received thrombolytic therapy and is being aggressively treated with anticoagulation or antiplatelet agents. Insertion of the pacemaker by a cutdown or the right internal jugular may be associated with significant bleeding in such patients.

5. When there is no informed consent, unless temporary pacing is considered life-saving

Procedure basics:

Continuous electrocardiographic monitoring is recommended. Fluoroscopy is desirable, safer, and insures proper placement under direct fluoroscopic guidance, but is not always feasible. If fluoroscopy is not available, a balloon-tipped catheter is recommended as long as the patient has intact circulation to help “float” the pacemaker wire to the desired location within the right ventricle.

Access site- the best access site for temporary pacing is via the left subclavian vein or right internal jugular vein. Brachial and femoral vein approaches are not recommended because of the risk of cardiac puncture and instability using a brachial approach, and the risk of deep vein thrombosis and infection using the femoral approach. The right internal jugular and the left subclavian veins have the straightest anatomic pathway to the right ventricle and are generally preferred for transvenous pacing. You will need an introducer set or sheath. Some pacing catheters are prepackaged with the appropriate equipment, others require a separate set. The introducer sheath must be larger than the pacing wire to allow it to pass!

Obtain pacing generator:

The rate control or (top control) is where you set the rate or beats per minute.

The ouput control (middle control) allows the operator to vary the amount of electrical current (amperage, amps) delivered to the myocardium; increasing this setting increases the output and improves the likelihood of capture.

The pacing control/sensitivity (the most inferior control), is determined by adjusting the gain setting for the sensing function of the generator. By increasing the sensitivity one can convert the unit from a fixed-rate (asynchronous mode) to a demand (synchronous mode) pacemaker. The voltage setting represents the minimum strength of electrical signal that the pacer is able to detect. Decreasing the setting increases the sensitivity and improves the likelihood of sensing myocardial depolarization.

In the fixed-rate mode(asynchronous) the unit fires despite the underlying intrinsic rhythm, the unit does not sense any intrinsic electrical activity. In the full demand mode, (synchronous mode similar idea to synchronized cardioversion) the pacemaker senses the underlying ventricular depolarizations and the unit does not fire as long as the patients ventricular rate is equal to or faster than the set rate of the pacing generator.

Initial settings: Set Rate (80 beats/min or 10 beats faster than the underlying ventricular rhythm, output 5 mA, sensitivity 3 mV)

Obtain central venous access with an introducer. Attach the still-compressed sterile sheath to the introducer hub (make sure the connector of the sheath is firmly attached to the hub of the introducer), open the hub of the introducer by turning it counter clockwise to allow passage of the pacing wire.

Inflate then deflate the balloon on the pacing wire before it is introduced to test for integrity. There is a valve that keeps the balloon inflated; it must be turned to inflate /deflate the balloon. Use 1.2-1.5 mL of air for the balloon. An assistant attaches the proximal pacing wire to the nonsterile energy source. Use the demand mode and turn on the pacer output to the highest level, rate about 80/min, with the balloon deflated.

Insert the pacing wire into the still collapsed sheath and into the hub of the introducer. Slowly advance the wire through the introducer. Inflate the balloon when the tip of the pacing wire is in the superior vena cava (10-12 cm) and continue to advance. Close the valve to keep the to keep the balloon inflated. Watch the ECG and look for capture, demonstrated by a wide QRS pattern after each pacer spike. The right ventricle should be encountered by 15-20 cm as noted by markings on the pacer wire. If no capture is seen by 25 cm, deflate the balloon, withdraw the wire and try again. When consistent capture is seen, deflate the balloon and advance the wire 1-2 cm more to seat the wire in the endocardium. Tighten the valve on the sheath introducer to stop subsequent movement of the wire, and extend the sheath its full length. If required suture the wire in place. The lead should be tied down in at least two different sites, one where the lead exits from the skin and other to a loop formed with the lead.

Turn down the output control (middle control), then slowly turn it up to determine pacing threshold (first sign of capture). Set the output at two to three times the stimulation threshold and set the desired rate. Leave the pacer in the demand mode until stability is assured.  Obtain chest x-ray and 12-lead EKG.

EKG Guidance: The patient should be connected to the limb leads of an EKG machine, The pacemaker may be attached to any of the V leads (usually V1 or V5)

When the pacing wire enters the superior vena cava (10-12 cm for a subclavian or internal jugular insertion) the balloon is inflated.

The V lead ( usually V1 or V5) should be monitored. The P wave and QRS complex should be observed to ascertain the position of the catheter tip. As the pacing wire passes through the tricuspid valve, the P-wave becomes smaller and the QRS complex becomes larger. After successful passage of the pacing wire into the right ventricle, the tip should be advanced until contact is made with the endocardial wall. When this occurs, the QRS segment will show ST segment elevation.

Complications related to Central Venous Catheterization:

1.            Inadvertent arterial puncture (compress)

2.            Venous thrombosis and thrombophlebitis uncommon (Femoral vein thrombosis             more common)

3.            Pneumothorax

4.            Hemothorax

5.            Thoracic duct laceration chylothorax (left-sided insertion)

6.            Air embolism

7.            Wound infection

8.            Pneumomediastinum

9.            Hydromediastinum, hemomediastinum

10.            Phrenic nerve injury

11.            Fracture of guide wire and embolization

Complications of right-sided heart catheterization:

1.            Dysrhthymia with pvc’s bing a common occurrence

2.            Ventricular tachycardia

3.            Pacer in pulmonary artery

4.            Pacer in coronary sinus

5.            Left ventricle through ASD,VSD

6.            Septal puncture

7.            Extraluminal insertion

8.            Arterial insertion

9.            Perforation of the ventricle can result in loss of capture, hemopericardium,             tamponade

10.            Local infection

11.            Balloon rupture

12.            Pulmonary infarction

13.            Phrenic nerve pacing

14.            Rupture of the chordae tindinae

Defibrillation and cardioversion are safe in patients who have temporary pacemakers

References:

1. Roberts: Clinical Procedures in Emergency Medicine, 5th ed; 2009

1. UpToDate: temporary cardiac pacing; 2012
2. LearnTheHeart.com

Case Presentation by Dr. Brandon Cheppa

Chief Complaint: “My foot hurts”

History of Present Illness:  This is a 40 year old male with a one day history of sudden right foot pain.  He states that last night he jumped over a fence and upon landing he had sudden onset of pain in his foot.  He states that he has barely been able to put weight on his foot and that walking is difficult.  The pain is constant, worsening, and he has never had pain in his foot like this before.  He denies any knee, hip, or back pain.  He denies any history of pain in any of his other joints.  He denies any head trauma, loss of consciousness, or numbness in any of his extremities.  He has not tried any medications and nothing seems to make it better or worse.

Review of Systems:  As per HPI

Past Medical, Family, and (or) social history:

Past Medical History:  Negative for Hypertension, Negative for diabetes

Past Surgical History: Denies any surgeries

Medications: None

Allergies: No known drug allergies

Social History:  Smokes cigarettes, denies alcohol, drugs, or intravenous drug use.

Family History: Unknown

Examination of organ system and body areas:

Vital signs: BP: 136/97, HR: 88, RR: 18, Temp 36.7 orally

Constitutional:  Patient appears comfortable, sitting in a wheelchair

HEENT:  Head is normocephalic, atraumatic, no tenderness to palpation, PERRLA, EOMI,

Neck:  Soft, supple, no masses, no cervical midlinetenderness

Cardiovascular:  Normal heart sounds

Respiratory:  Normal breathsounds

Gastrointestinal:  Soft, non-tender, non-distended, no palpable masses

Skin: No lacerations, no open lesions, no rashes seen

Neurological:  Patient is AOx3, acting appropriately, No sensory deficits,  grossly moving all extremities well, normal facial symmetry.  He has a hobbling gait favoring his left side and is unable to put weight on his right leg.

Back: No midline tenderness of entire spine

Skin:  No ecchymosis or breaks in skin seen

Musculoskeletal:  Upper extremities and Left lower extremities have full range of motion at all joints with 5/5 strength to flexion and extension and have no swelling or deformities to palpation.  Focused exam of left lower extremity:  Full range of motion of hip and knee with 5/5 strength to flexion and extension.  Patient has no calf tenderness, no Achilles tendon tenderness.  Right ankle has no malleolar tenderness.  He has tenderness of his midfoot, it is red, swollen with no crepetus or fluctuence.  He has good symmetrical pules of both feet with good capillary refill and he is neurovascularly intact.

Labs: None

Images: Complete x-ray of the foot was obtained

Questions:

1) The x-ray obtained is concerning for which type of fracture?

A. Boxer’s fracture

B. Jones’ fracture

C. Lisfranc’s fracture

D. Maisonneuve fracture

E. Salter-Harris type IV fracture

2) What is the appropriate disposition for the patient?

A.  Ace wrap, crutches, non-weight baring, follow-up with orthopedic clinic in 1 week

B.  Ace wrap, “ortho shoe”, weight bare as tolerated, follow-up with orthopedic clinic in 1 week

C.  Immediate orthopedic consultation in the emergency department

D.  Posterior mold splint, crutches, non-weight baring, follow-up with orthopedic clinic the next day

3) What is the most common complication this patient will experience if this injury is not appropriately treated?

A.  Compartment syndrome

B.  Deep Venous Thrombosis

C.  Degenerative Arthritis

D.  Osteomyelitis

E.   Regional Pain Syndrome

Answers:

1)    C

2)    C

3)    C

Discussion:

A Lisfranc fracture is one part of the collective term Lisfranc Injury.  A Lisfranc injury can very in radiographic presentations, but are all centered around any injury to the tarsometatarsal joints, also known as Lisfranc’s joint.

The Lisfranc’s Joint is made up of the five metatarsals and their articulations with the three cuneiforms, the navicular bone, and the cuboid bone.  The biomechanical structure of the foot allows for passage of neurovascular bundles and connective tissues through the foot without being crushed by a person’s weight.  The metatarsal bones have a trapezoid shape and are arranged in an arch configuration using the second metatarsal as the “keystone”.  Under normal physiologic conditions the second metatarsal has very little motion compared to the other four metatarsal bones.

The Lisfranc ligament is the strongest of the tarsometarsal ligaments and connects the lateral surface of the medial cuneiform to the medial base of the fifth metatarsal.  There are no proximal ligaments between the bases of the first and second metatarsals, most likely due to the evolution of the foot from a primitive hand structure where the first metatarsal evolved from a primitive thumb.  There are ligamentous connections between the second through fifth metatarsal bones and all five have distal ligamentous connections.  One to two mm of dorsolateral displacement of the affected base of the second metatarsal can lead to 13-25% reduction of contact at the joint.  The dorsalis pedis artery and deep peroneal nerve can be compromised with this injury due to their locations in the foot.

Patients can injure this structure by many mechanisms and it usually results in a closed fracture.  Motor vehicle collisions, falls, and even pedestrians tripping on curbs can produce this injury.  It stems from forceful abduction of the forefoot of a plantar-flexed foot.  Windsurfers, motorcyclists, and people who get thrown off horses have been historically at risk for this injury.  Patients typically will present with pain, swelling to the midfoot, and difficulty placing weight on the injured extremity.  They may present with ecchymosis to the plantar surface of the midfoot, although not specific, it is suggestive of an injury.  A detailed history and physical exam with attention to other associated injuries such as at the knees, hips, and lower back will guide your work-up.

Complete x-rays of the foot will pick up a Lisfranc injury 90% of the time.  With high clinical suspicion, and a presumptive negative x-ray, you can elect to get “stress” views of the foot which requires the patient to place weight on the injured foot.  Often times this is difficult to accomplish due to significant pain, or lack of ability to interpret a “stressed-view” of a foot x-ray, therefore a CT scan will aid in diagnosis.

With the knowledge of the anatomy combined with the mechanism of force, on radiograph, a fracture at the base of the second metatarsal is pathognomonic of a disruption of the Lisfranc ligamentous complex.  The diagnosis is made radiographically on the anteriorposterior view when there is a gap greater than 1 mm between the bases of the first and second metatarsals.  Other radiographic findings may be present or can lend to the diagnosis such as loss of alignment of the medial edge of the base of the second metatarsal with the medial edge of the middle cuneiform; loss of alignment of the lateral border of the third metatarsal shift with the lateral border of the lateral cuneiform; or loss of alignment of the medial border of the fourth metatarsal with the medial border of the cuboid.  If radiographs are unequivocal, and suspicion is still high, there is a chance of a spontaneously reduced dislocation.

Patient who sustain a Lisfranc injury require an emergency room orthopedic consultation and are to be made non-weight baring until their evaluation.  This is due to the large degree of instability of the joint that could lead to significant disability, and the potential for compartment syndrome and/or neurovascular injury.  Patients typically need to go to the operating room and undergo open or closed reduction with application of hardware.  Patients who have a Lisfranc sprain, will require below-knee casting, crutches, “RICE” therapy, and close orthopedic follow-up due to their potential for operative fixation.

The most common complication of an untreated Lisfranc injury is degenerative arthritis in the form of posttraumatic arthrosis.  Other less common complications include: compartment syndrome in the acute injury setting, deep venous thrombosis due to the amount of immobility, regional pain syndrome.

With early diagnosis and proper orthopedic intervention, 95% of patients at 3.5 years will have an excellent outcome.

The case revisited:

This gentlemen raised our suspicion for a midfoot injury based on his mechanism and physical exam.  We obtained foot radiographs and it showed a fracture of the base of the second metatarsal (circled in green), widening between the bases of the first and second metatarsal (measurement in blue), and a “fleck sign” (circled in red) which is a ligamentous disruption from the base of the second metatarsal.  This radiograph raised our suspicion for a Lisfranc injury and the orthopedic service was consulted.

They requested a CT scan due to the high potential for other associated fractures and it also showed a comminuted fracture of the medial cuneiform bone.

They opted to not take him for emergent surgery due to him having an ongoing underlying infection which was unknown during the initial patient encounter.  On reassessment, the patient had been experiencing painless, white discharge from his penis for the last two months.  The orthopedic service felt his infection could complicate his healing due to the chance that hardware will need to be applied during surgery.  They placed him in a cast, made him non-weight baring, and wanted him to follow-up in their clinic when his infection had resolved.  He was swabbed for Gonorrhea and Chlamydia, and treated for both of those infections including Trichomonas.  The results of his cultures were negative making Trichomonas the most likely cause of his infection.  At a follow-up visit in the orthopedic clinic, they felt there was not significant boney displacement and took him to the operating room to achieve “stressed” views of the foot under anesthesia.  They were satisfied with the stability of the joint and did not undergo any surgical intervention.  He was placed him in a non-weight baring cast and will continue to follow-up in the orthopedic clinic.

References:

Rosen’s, 7^th edition, pp 681-695

Tintinalli’s, 6^th edition, pp 1742-1746

Browner: Skeletal Trauma, 4^th edition, 2008, Foot Trauma chapter

Ouzounian T.J., Shereff M.J.: In vitro determination of midfoot motion.  Foot Ankle  1989; 10:140-146.

Lu J., Ebraheim N.A., Skie M., et al: Radiographic and computed tomographic evaluation of Lisfranc dislocation: A cadaver study.  Foot Ankle Int  1997; 18:351-355.

Case Presentation by Dr. Claire Jensen

CC: “I have a fever.”

HPI: This is a 61 year-old Caucasian female with recently diagnosed squamous cell carcinoma of the base of the tongue who presents to the Emergency Department after noting a fever of 101.9° F at home approximately one hour ago. She is currently undergoing induction chemotherapy with docetaxel, cisplatin, and 5-FU. She completed her third cycle of chemotherapy 8 days ago, which was administered in the inpatient setting. Prior to hospital discharge, she received a dose of pegfilgrastim for anticipated neutropenia. Apparently, her tumor has responded well to chemotherapy and she is tentatively scheduled to undergo neck dissection with tumor resection in the next four weeks. Her chemotherapy course has been complicated by problems with nausea and mucositis.

She states that she has been seen in her oncologist’s office both earlier today and yesterday for complaints of generalized weakness and twice received infusion of intravenous fluids for “low blood pressure.”  She states that she had just returned home from her doctor’s office late this afternoon when she started to feel very cold. She took her temperature, noted the fever, and returned immediately to the hospital on her doctor’s instruction. She has chronic cough since undergoing tracheostomy, but denies changes in sputum. No chest pain or shortness of breath. She denies dysuria or urinary frequency. She reports nausea and diarrhea associated with this most recent round of chemotherapy, but denies melena or hematochezia.

ROS: Per HPI.

PMH: Asthma, T3N2cM0 squamous cell carcinoma of the base of the tongue.

PSH: Hysterectomy, fine-needle aspiration of neck mass, triple endoscopy and tracheostomy, Medi-Port placement.

Allergies: Codeine and shellfish

Medications: Ondansetron, prochlorperazine, acetaminophen/hydrocodone, diazepam, esomeprazole, fluticasone/salmeterol inhaler, docusate, fexofenadine.

FH: Cancer, hypertension, diabetes, “thyroid problems.”

SH: Remote history of tobacco abuse, quit smoking 21 years ago. Denies alcohol or illicit drug abuse.

PE:

General:.This is a well-developed, thin female. She is awake and alert. She answers questions appropriately and speaks in full sentences. She is mildly ill-appearing.

Vitals: BP 132/74, P 128, R 18, T 38.6 C, SpO2 100% on room air

Eyes: There is mild conjunctival pallor, no injections, sclerae anicteric. Pupils and equal and reactive. Extraocular movements are full.

Ear, Nose, Mouth and Throat: Tympanic membranes are normal in appearance bilaterally. There is no nasal drainage, no sinus tenderness. The oropharynx has slightly dry mucous membranes. There is mild mucositis, no candidiasis. Good dentition.

Neck: Supple, no lymphadenopathy, no JVD. Uncuffed tracheostomy tube without purulent secretions, no erythema or drainage at insertion site.

Cardiovascular: Tachycardic, normal S₁, S₂. No murmurs, rubs, gallops. No lower extremity edema or calf tenderness.

Respiratory: Lungs are clear to auscultation bilaterally with good air entry.

Gastrointestinal: The abdomen is flat, soft, non-tender and non-distended. Bowel sounds are present.

GU: Deferred.

Musculoskeletal: The head is normocephalic and atraumatic. No tenderness over the neck or spine. There is normal muscle bulk and tone. No erythema or swelling of the joints.

Skin: Warm and dry. No rashes, bruising or diaphoresis. The skin over the Medi-port is without induration

Neurologic: Awake and alert. Symmetric facies. Normal speech. Moves all extremities spontaneously. Sensation intact to light touch in all extremities. Normal gait.

Laboratory Studies:

WBC:                                   0.8

Hgb:                                    8.0

Hct:                                    22.8

Plt:                                     104

Myelocytes:                        0%

Metamyelocytes:              4%

Bands:                                0%

Neutrophils:                    14%

Lymphocytes:                 34%

Monocytes:                     46%

Eosinophils:                     2%

Basophils:                         0%

Na:                                   130

K:                                          3.9

Cl:                                      98

CO₂:                                  21

BUN:                                15

Cr:                                      1.0

Glu:                               151

Ca:                                    8.4

Mg:                                   1.3

AST:                               27

ALT:                               11

Alk Phos:                      91

Total Protein:                6.1

Albumin:                         3.2

Lactic Acid:                    2.2

Urinalysis

Glucose                        1+

Ketones                        Negative

Blood                             1+

Bilirubin                       Negative

Specific Gravity           1.015

pH                                  6.5

Protein                           Negative

Nitrite                            Negative

LE                                   Negative

RBCs                                    2-5

WBCs                                   <5

Epithelials                          <5

Casts                               None

Crystals                          None

Bacteria                          None seen

Chest X-Ray

Emphesematous lungs. Normal heart size. No active parenchymal disease. Medi-Port and tracheostomy tubes in stable position.

Questions

1.     What is the patient’s absolute neutrophil count?

a) 12

b) 112

c) 1120

d) 11200

2.  Which of the following parenteral antibiotics is considered first-line therapy for the high-risk febrile neutropenia patient?

a) Cefepime

b) Ciprofloxacin

c) Metronidazole

d) Tobramycin

e) Vancomycin

3.  Which factor is associated with “low risk” febrile neutropenia patients, who may be candidates for outpatient antibiotic therapy after careful consideration?

a) Age >60 years

b) Hematologic malignancy

c) Predominance of gastrointestinal symptoms, such as nausea, vomiting, diarrhea, or           abdominal pain.

d) Presence of underlying structural lung disease, such as COPD.

e) Solid tumors

Answers:

1. B, 2. A, 3. E

Discussion:

Febrile neutropenia is a medical emergency that requires a rapid and methodical response from the emergency physician. Prior to the era of empiric antibiotic therapy, infection accounted for almost 75 percent of mortality associated with chemotherapy. The definition of neutropenia varies between institutions, but is typically defined as an absolute neutrophil count of less than 500 cells/microL, or less than 1000 cells/microL with a predicted nadir of less than 500 cells/microL. Profound neutropenia is defined as less than or equal to 100 cells/microL.

The absolute neutrophil count is calculated by multiplying the total white blood cell count by the percentage of neutrophils and bands.

ANC = (WBC count in 1000s) x [(% Neutrophils/100) + (% Bands/100)

So, in our patient:

ANC = (0.8 x 1000) x ((14/100) + (0/100)

= 800 x 0.14

= 112

Multiple factors are used to categorize patients as high-risk or low-risk for severe infection and include presenting signs and symptoms, the type of underlying malignancy, the type of therapy for the underlying cancer, and the presence of medical comorbidities. Significant comorbidities include uncontrolled cancer, COPD, poor functional status, and advanced age. Patients undergoing induction chemotherapy for acute myelogenous leukemia or a chemotherapeutic conditioning regimen in preparation for hematopoeitic stem cell transplantation are at particularly high risk.  Patients with an ANC <100, hemodynamic instability, GI symptoms such as abdominal pain, nausea, vomiting or diarrhea, new-onset neurological symptoms including altered mental status, underlying chronic lung disease, or evidence of hepatic or renal dysfunction are all considered high risk and should be admitted to the hospital for empiric antibiotic therapy. Additionally, it is important to observe neutropenic precautions when the patient is in the emergency department, with placement in a private room if available, use of masks by staff members, and adherence to rigorous hand hygiene. Patients with solid tumors, anticipated short duration of neutropenia (<7 days), and lack of comorbid conditions can be considered for outpatient antibiotic therapy under close supervision, but only after thorough diagnostic evaluation and discussion with their managing oncologist.

Initial evaluation and management of these patients in the emergency department is not tremendously different from that of the septic patient. Emphasis is on immediate and aggressive correction of hemodynamic instability, identification of potential sources using diagnostic studies, early administration of empiric antibiotics, and source control (venous catheters, ports, urinary catheters, etc.). However, it is important to be mindful that severely neutropenic patients are not capable of mounting an immune response the way septic patients are, so a negative chest x-ray or absence of pyuria on urinalysis does not necessarily exclude infection. Standard diagnostic work-up includes CBC with differential, electrolyte studies including renal function, transaminases to assess for hepatic insufficiency, two sets of blood cultures with one from any indwelling catheter if present, chest radiograph, and urinalysis with urine culture. The need for additional studies such as other imaging, lumbar puncture, or fungal cultures are not standard, but should be considered on a case-by-case basis. Neutropenic patients that are afebrile but present with symptoms concerning for infectious illness such as hypothermia, hypotension, abdominal pain, or mental status changes should be treated as high-risk patients.

Early institution of antibiotic therapy is of utmost importance in the setting of febrile neutropenia. Early studies documented mortality rates as high as 70 percent in cases where the administration of empiric antibiotics was delayed. Therapy should be tailored based upon known or suspected sources of infection, the patient’s history as well as any previous culture data or recent antibiotic use, and awareness of institutional nosocomial infection patterns. The Infectious Disease Society of America issued new guidelines in 2010 for the treatment of neutropenic fever, which includes the initiation of monotherapy with an anti-Pseudomonal beta-lactam agent such as cefepime, meropenem, imipenem, or piperacillin-tazobactam. Other antibiotics such as aminoglycosides, fluoroquinolones and/or vancomycin may be added in patients with complicated infections (eg, hypotension or mental status changes) or if antimicrobial resistance is suspected. Vancomycin and other agents that target gram positive organisms are not recommended as part of the standard initial management unless there is suspicion for catheter-related blood stream infection, skin or soft tissue infection, pneumonia or hemodynamic instability is present.

This patient was started on empiric antibiotic therapy with cefepime and vancomycin and admitted to the hospital. She had no further febrile episodes while in the hospital. Her WBC counts started rebounding the next day, and all of her cultures showed no growth. She was discharged in good condition after three days in the hospital and is currently still on schedule to undergo surgical resection of her tumor.

Case Presentation by Dr. Sarah Albers

CHIEF COMPLAINT(S):

“She has got a fever and is throwing up.”

HISTORY OF PRESENT ILLNESS:

A 16-year-old Caucasian female presents with both of her parents to the emergency department.  The adolescent girl complains of “not feeling well over the past one day.”  She feels dizzy, which she describes further as persistent wooziness that is not positional; there is no sensation that she or the room is spinning. She also feels nauseous, and has a headache – described as a tight band around her temples, with no blurriness of her vision, or change in her vision or hearing. No history of trauma or falls.  She also has generalized myalgias, a sunburn like rash over her trunk, back and upper extremities, redness to her eyes, chills and a fever that started abruptly a couple of hours ago; her temperature was 104 F at home and she took Tylenol, but then vomited it back up.  She states that it hurts her muscles when she takes a deep breath.  She has had no cough or chest pain. She denies shortness of breath or difficulty breathing. No runny nose or sore throat.  No leg pain.  She says she is just feeling “generally weak and my whole body hurts.”

She has had nausea and vomiting today, approximately 10 to 20 episodes of emesis that have been nonbloody, nonbilious.  She has been unable to keep anything down except for a little bit of water and ice chips.  She denies any abdominal pain, blood in her stools, or any black tarry stools.  She states she has bowel movements regularly; her last bowel movement was today with no diarrhea or constipation.  She denies any dysuria, urgency or frequency.  She denies any vaginal discharge, but is currently on her period.

She said she started feeling a little bit “bad” last night with the beginning of a headache; however, today was when everything “hit” her.  She describes as all of these symptoms coming on suddenly.  Mom states she has not been hospitalized nor has she been treated with antibiotics over the past 2 months.  Two months ago she was treated for pneumonia.  She is currently on a homoeopathic medication for Candida called Threelac.  Otherwise, this child is healthy and takes no medications. She has no known sick contacts.

REVIEW OF SYSTEMS:

CONSTITUTIONAL:  Positive fever & chills.

EYES:  No change in vision.  Positive red eyes.

ENT:  No change in hearing, runny nose, or sore throat.

RESPIRATORY:  No wheezing, cough, or hemoptysis.

CARDIOVASCULAR:  generalized muscle soreness of her chest wall when taking deep breaths, otherwise no pain.  No palpitations or edema.

GI:  Positive nausea & vomiting.  No diarrhea or constipation.  No black tarry stools or bright red blood per rectum.

GU:  No dysuria, urgency, or frequency.  She is currently on her menstrual cycle.  She does use tampons, and currently has one in.

MUSCULOSKELETAL:  Positive myalgias.  No injury or trauma.

SKIN:  Positive erythematous rash over her trunk, arms, and back.

CNS:  Generalized weakness, no syncope, numbness, speech deficit, confusion or altered mental status.

PAST MEDICAL, FAMILY, AND(OR) SOCIAL HISTORY:

PAST MEDICAL HISTORY:  None.  However, recent treatment for pneumonia and the patient is currently being treated with a homeopathic medication for a possible candida infection.

PAST SURGICAL HISTORY:  None.

MEDICATIONS:  Include a homeopathic called Threelac to treat Candida.  She is also taking a “digestive enzyme”.

ALLERGIES:  NO KNOWN DRUG ALLERGIES.

FAMILY HISTORY:  negative for hypertension or diabetes

SOCIAL HISTORY:  Negative for tobacco, alcohol, and drugs.  The patient is not currently sexually active.  She has never had sex in the past.  They do have working smoke detectors in the house.  She does always wear a seatbelt in the car.  There are no guns in the house. She does do well in school.

EXAMINATION OF ORGAN SYSTEMS-BODY AREAS:

VITAL SIGNS:  On arrival, her blood pressure 111/90, heart rate of 122, respiratory rate is 18, temperature is 39 orally, pulse ox is 95% on room air.

CONSTITUTIONAL AND GENERAL:  The patient is a tall, thin, well-developed, well-nourished female, in no acute respiratory distress, speaking in full sentences, cooperative for exam, A and O x3. She is nontoxic appearing.  She smiles on exam and converses with her parents and me and jokes around a bit. She is sitting upright on the stretcher with her legs drawn up in front of her with her arms wrapped around her legs.  She is wearing a patient gown.  She does have slightly reddened eyes as well as reddish hue to her arms on observation.

HEENT:  Head is normocephalic, atraumatic.  No acute masses or lesions.  Eyes:  Pupils are 3 mm, round and reactive to light.  Extraocular movements are intact.  No conjunctival pallor.  Sclerae are anicteric.  Sclerae are also injected bilaterally.  No evidence of discharge in her eyes.  Nose: no nasal discharge is noted.  Ears:  Tympanic membranes are clear bilaterally. Landmarks are clearly visualized. Mouth and throat:  Mucous membranes are moist.  No erythema, tonsillar exudates or intraoral lesions.

NECK:  Supple.  No lymphadenopathy.  No thyromegaly.  No tenderness to palpation of the cervical spine.  Trachea is midline.  No meningismus or nuchal rigidity.

LUNGS:  Clear to auscultation bilaterally.  No wheezes, rales or rhonchi.  Good air exchange in all lung fields.

HEART:  S1, S2 are present.  Tachycardic rate and regular rhythm, pulses in all four extremities are equal and 2+.

BACK:  No cervical, thoracic, lumbar or sacral spinal tenderness.  The patient has no CVA tenderness.

EXTREMITIES:  No clubbing, cyanosis or edema.

SKIN: The patient does have an erythematous, first degree sunburn-looking rash on the anterior aspect of her bilateral upper extremities as well as her anterior and posterior chest and abdominal wall.  It is blanching in nature.  There are a few very tiny papules on the area of her anterior forearm.  There is no sloughing of skin or bullae formation.  There is no blistering of the skin.  Skin is not tender to touch.  Skin is warm to touch throughout.  She has no erythema or rash on her palms or soles.  She has no rash or erythema on her bilateral lower extremities.

GU:  Performed in the presence of a female nurse chaperone shows normal, Tanner Stage 5, female external genitalia. On speculum exam a tiny amount of blood in the vaginal vault, patient is currently menstruating.  No tampon is present. There is a closed cervical os.  The patient does have pain on insertion of the speculum.  Swabs were obtained. The patient does have cervical motion tenderness as well as bilateral adnexal tenderness. No masses were palpitated. There are no excoriations or sores on the inside of the vaginal vault. Microscopy was negative for trichomonas or clue cells.

NEUROLOGIC:  The patient is awake, alert, and oriented x3.  Normal speech and hearing to finger rub.  Face is symmetrical.  No nystagmus is present.  Sensation is equal and intact throughout.  Motor strength is 5/5 in all four extremities.  The patient does ambulate with a normal gait.

Questions:

1)    At what point does the accepting hospital assume responsibility for a transfer patient?

• a.  as soon as the transporting service (ambulance, helicopter) reaches the accepting hospital grounds
• b.  half-way through transit, when the accepting facility is closer than the  sending facility
• c.  when the patient arrives inside the accepting facility doors
• d.  when the patient leaves the sending facility

2)    Which of the following is most likely to predispose a patient to this condition?

• a.  niacin use
• b.  recent antibiotic use
• c.  recent seafood ingestion
• d.  tampon use

3)    What condition is the patient most likely suffering from?

• a.  drug-induced dermatitis
• b.  Stevens-Johnson syndrome
• c.  toxic epidermal necrolysis
• d.  toxic shock syndrome

Answers:

1. d

2. d

3. d (Staph Aureus) Toxic shock syndrome from tampon use

Discussion:

Toxic Shock Syndrome (TSS) is characterized by severe prolonged shock and is caused by a toxin produced by S. Aureus. This was originally described by Todd et al. in 1978.  They reported a series of 7 cases of kids 8-17, S. Aureus was cultured from various body sites, but not the blood, in 5 of the 7 cases.  Most of the subsequent cases have occurred in menstruating females often after a menstrual period associated with tampon use.  In the early 1980’s the consistency of tampons were changed to reduce absorbancy due to growing concerns about TSS.  In the late 1980’s group A Streptococcal toxic shock syndrome (strep TSS) was described because it shares so many feature with TSS.

Menstruation and tampon use is the most common setting for TSS, but non-menstruation TSS accounts for just under half of the reported cases.  Of these cases, strep TSS account for just over half of the cases. Nonmenstrual TSS is associated with super infections of skin including burns, surgical sites, dialysis catheters and lung (influenza associated). It can also happened in association with staph respiratory infections or colonization without an obvious infection source. Strep TSS is classically associated with more severe soft tissue infections including necrotizing fasciitis and myositis, as well as pneumonia, peritonitis, myometritis and osteomyelitis. Mortality reaches 30-70% in strep TSS, and in staph TSS it is <3%.

Staph TSS is caused by the colonization or infection with toxigenic strains, specifically TSST-1 (toxic shock syndrome toxin – 1). Because the organism is not invasive, blood cultures are often negative. Strep TSS is caused by invasive infection with toxigenic strains of GAS (Group A Strep).

The clinical presentation of Strep TSS and staph TSS is similar. The primary difference is that an identifiable source is virtually always present with strep TSS and colonization alone may lead to staph TSS.

Clinical presentation:

Patients may present with fever, chills, nausea, vomiting, diarrhea, headache, myalgias, and pharyngitis.  Prodrome may last hours to 2 or 3 days. The fever is usally high and abrupt in onset (although septic patients may be hypothermic).  The classic rash is a nonpuritic, diffuse, blanching, macular erythroderma.  Initially, this may be mistaken as flushing due to fever.  The rash is typically diffuse but may be localized to the trunk, extremities or perineum.  After about a week a fine flaking desquamation occurs of the face, trunk and extremities followed by full thickness peeling of palms, soles and fingers. This classic rash is much more common with staph TSS and is present in less than 10% of patients with strep TSS.

TSS Rash

Toxic shock syndrome. A. Appearance of the rash associated with staphylococcal toxic shock syndrome (TSS). B. Gangrenous toes associated with prolonged hypotension in TSS. C. Desquamation of the skin that occurs during the resolution of TSS.

http://5minuteconsult.com/ViewImage/2027438

The patient’s mental status is frequently abnormal, out of proportion to the hypotension that ensues. Confusion, somnolence, agitiation and combativeness are present in 55% of strep TSS and even more frequent in patients with staph TSS. Other physical findings include pharyngeal and conjunctival erythema, strawberry tongue and peripheral edema. Vaginal mucosal erythema and purulent vaginal discharge may be present in menstrual TSS. As more organ systems become involved a wide range of signs and symptoms may be seen.  GI involvement manifests itself by nausea, vomiting, diarrhea and abdominal pain.  Hepatomegaly may be present. Patients may become hypoxic and develop rales on lung examination.

Comparison for staph and strep TSS

• Risk Factors for TSS
• tampon use
• postoperative wound infections
• postpartum period
• nasal packing
• cancer
• common bacterial infections
• ETOH abuse
• infection with influenza A
• infection with varicella
• Diabetes
• HIV
• Chronic cardiac disease
• Chronic pulmonary disease
• NSAID (may mask symptoms rather than be a risk factor)

Diagnosis:

 The case definition for TSS does not require a positive culture for S. Aureus, but a positive culture is required to diagnose strep TSS. Specific tests are not required to rule out other diseases, but if such tests are obtained the results must be negative.

No specific laboratory changes are associated with TSS, but many abnormalities are common including: leukocytosis or leukopenia, bandemia (very common), elevated creatinine and hemoglobinuria, hypoalbuminemia and hypocalcemia. Other abnormailities include anemia, thrombocytopenia, hyperbilirubinemia, elevated transaminase levels and sterile pyuria.

A lumbar puncture should be performed on febrile patients with altered mental status to evaluate for meningitis. It is prudent to wait for the coagulation profile before the LP, as DIC may exist at the time of presentation. The CSF is normal in TSS.

Management:

TSS patients should receive aggressive fluid resuscitation with crystalloids and may require up to 10-20 L a day! Supplemental oxygen should be provided to all septic patients regardless of initial pulse ox. This will allow for maximal tissue oxygenation and reduces acidosis. They should have continuous cardiac and pulse oximetry monitoring.

The source of bacteria (tampons, nasal packs and other foreign bodies) must be removed immediately.  (On our case patient, ROS stated tampon was in and on pelvic exam tampon was out).  Prompt surgical consultation should be obtained to debride wounds. If specimens are sent for culture, the lab should be informed of the suspected diagnosis.

Patients who do not respond to fluids require vasopressors.  Antibiotics (broad spectrum) need to be initiated early in TSS.  Clindamycin is recommended, as it is a potent suppressor of bacterial toxins (dose is 600-900 mg IV q 8h or peds dose is 20-40 mg/kg/day divided every 6-8 hours).

Disposition:

All patients thought to have TSS should be admitted to an ICU!  Again, prompt surgical intervention should be obtained for patients with a wound source.

So back to our patient…

16-year-old adolescent girl presenting with suspected TSS from tampon use.  We had her immediately remove her tampon.  (Note tampon in on ROS, but not during pelvic). On re-evaluation, repeat BP was 70/30-50’s and lab work returned showing:  elevated lactate, acute renal failure, leukocytosis, mild elevation in coags (PT/INR).

ID was consulted and recommended broad spectrum abx including clindamycin, vancomycin and ceftriaxone, which were all started. BP remained at 70’s systolic after 5 L of crystalloid fluids.  Fever and vomiting was controlled with IV NSAIDS and antiemetics.

Patient’s mental status remained AOx3 the entire time, she never looked toxic, continued to smile on exam and wanted to continually walk to the bathroom.  Decision was made to transfer to CHM PICU as a direct admission, CHM requested we not start pressors or a central line at our facility.  They did send PANDA to come get this patient by helicopter.  She ended up on three pressors; dobutamine, Dopamine and vasopressin (all were weaned by hospital day 3) at CHM in the PICU after a femoral line was placed.  Same antibiotics were continued.  Vaginal swab grew Staph Aureus (MSSA), GC and Chlamydia were negative. Blood cultures were negative.  Urine culture grew staph coagulase positive.  After three days in the PICU she was transferred to the ID service and then discharged after one day on the floor.  She was sent out with a 3-week course of clindamycin.  She developed C. Difficile colitis and was treated with oral flagyl and vancomycin.

Case Presentation by Dr. Jessica Ruffino

HPI: 25y/o female at 36 weeks GA presents to ED via EMS as a trauma code after MVA.  Patient was a restrained driver, airbags were deployed.  Patient states she was rear-ended while stopped at a traffic signal and hit the car in front of her.  Other vehicle was driving about 25mph.  Patient complains of abdominal pain mostly across lower abdomen.  Patient thinks she is having contractions, unsure of frequency.  Denies loss of fluid.  Last felt fetal movement prior to accident.  Patient denies chest pain, SOB, N/V.  Patient states her pregnancy has been uncomplicated, denies high blood pressure or diabetes.  Patient did not lose consciousness, was ambulating at scene per EMS.

ROS:  Negative except for stated in HPI

PMH:  G1P0.  Denies asthma, diabetes, hypertension

PSH:  None

Medications: Prenatal vitamins

Allergies: NKDA

SH:  Denies alcohol, tobacco, drug use.

Physical Examination:

Vital signs: BP 100/75, HR 100, RR 16, Temp. 36.9°, Pulse ox. 98% on RA

Constitutional: Patient is well nourished, gravid uterus.  No respiratory distress.  Appears anxious.

Head:  Normocephalic, atraumatic.  No tenderness to palpation.

Eyes:  Pupils 3mm bilaterally, round and reactive to light.  EOMI.  No conjunctival pallor.  No scleral icterus.

ENMT:  No hemotypmanum bilaterally.  No rhinorrhea or epistaxis.  Mucous membranes are moist.  No erythema or exudates in throat.

Neck:  In cervical collar.  No c-spine tenderness to palpation, no palpable deformities. Cardiovascular:  S1, S2.  Slightly tachycardic.  Regular rhythm.  No murmurs, rubs or gallops.

Respiratory:  Lungs CTAB.  No wheezes, rhonci or rales.  No tenderness over chest wall.  No palpable crepitus over chest wall or neck.

Gastrointestinal:  Gravid uterus.  Uterus is firm.  Fundus palpable about 15cm above umbilicus.  Tenderness to palpation in lower quadrants bilaterally.  Positive seatbelt sign across abdomen.

Genitourinary:  Sterile speculum exam showed small amount of bright red blood in vaginal canal.  Cervix is closed.

Musculoskeletal:  No TTP or deformities palpated along entire spine.  No obvious deformities.  No swelling.  No dependent edema.  2+ DP pulses bilaterally.

Skin:  No lacerations or rashes.  Positive seatbelt sign across abdomen.

Neuro:  Awake, alert and oriented x 3.  Normal speech.  Strength is 5/5 proximally and distally and bilateral upper and lower extremities.  Sensation to light touch intact throughout.  DTR’s 2+ bilaterally.

A FAST exam was performed and was negative.  Transabdominal ultrasound findings shown below.  FHTs in 140s-160s.

Questions:

1.  What is the most sensitive indicator of placental abruption?

a)  Ultrasound findings

b)  Fetal distress

c)  Vaginal bleeding

d)  Uterine tenderness

2.  Which of the following is true of resuscitation of a pregnant patient with uterus palpable at or above umbilicus who is in cardiopulmonary arrest?

a)  No modifications to resuscitative efforts should be made

b)  Chest compressions should be performed higher on sternum

c)  Manual displacement of uterus to the left should be attempted

d)  Defibrillation is contraindicated

3.  A pregnant patient may lose how much circulating blood volume before manifesting hypotension or clinical signs of shock?

a)  30-35%

b)  10-15%

c)  20-25%

d)  40-45%

Correct Answers:

1. B
2. C
3. A

Discussion:

Trauma occurs in 6 to 7% of all pregnancies.  It is the leading cause of maternal death due to nonobstetric causes, accounting for close to 50% of fatalities in pregnant women.  The most common causes of injury in pregnancy, in order of frequency, that result in emergency department (ED) visits are motor vehicle crashes (MVCs), interpersonal violence, and falls.  Counseling on proper seatbelt and alcohol use and screening for interpersonal violence may help to reduce the morbidity and mortality rates for pregnant patients.  Although the essential principles of trauma management remain unchanged in the pregnant patient, a number of special points need to be considered.  Pregnancy causes alterations in physiology and anatomy that affect multiple organ systems. Although there are two lives involved, maternal life takes priority.

In blunt trauma, 50 to 70% of all fetal losses result from placental abruption.  Placental separation results when the inelastic placenta shears away from the elastic uterus during sudden deformation of the uterus. Because deceleration forces can be as damaging to the placenta as direct uterine trauma, abruption can occur with little or no external sign of injury to the abdominal wall.  Because all gas exchange between the mother and fetus occurs across the placenta, abruption inhibits the flow of oxygen to the fetus and causes in utero CO₂ accumulation. Such hypoxia and acidosis can lead to fetal distress.  Sustained uterine contractions induced by intrauterine hemorrhage also inhibit uterine blood flow, further contributing to fetal hypoxia.

The diagnosis of abruption is a clinical one, and ultrasonography and the Kleihauer-Betke test are of limited value.  Classical clinical findings of abruption may include vaginal bleeding, abdominal cramps, uterine tenderness, maternal hypovolemia (up to 2 L of blood can accumulate in the gravid uterus), or a change in the fetal heart rate. However, in some trauma studies, as many as 63% of cases showed no evidence of vaginal bleeding.

The most sensitive indicator of placental abruption is fetal distress. Hence, prompt fetal monitoring is a very important assessment technique in trauma during pregnancy. There is also a close linkage of abruption to uterine activity. One study reported that if 12 or more contractions occurred in any hour of a 4-hour cardiotocographic monitoring period, the risk of abruption was 14%; abruption did not occur in this study if contractions occurred less than once every 10 minutes.  Ultrasound (US) is less than 50% accurate as a first-line test in detecting placental abruption.  If the abruption bleeds externally, not enough blood collects to be seen sonographically. Even with significant intrauterine blood accumulation, accurate US diagnosis may be difficult because of placental position (i.e., posterior) and confounding uterine or placental structural conditions.

Hemodynamic Changes of Pregnancy (Mean Values)

The relative hypervolemic state can mislead the clinician during maternal resuscitation after trauma and make clinical findings difficult to interpret.  A pregnant patient may lose 30% to 35% of circulating blood volume before manifesting hypotension or clinical signs of shock.  Uterine arteries constrict, which results in diminished fetal blood flow and tissue oxygenation before significant evidence of maternal hypovolemia appears.

Cardiopulmonary arrest in a pregnant patient must be considered under two scenarios: before fetal viability and after fetal viability. The accepted age of fetal viability varies among institutions, but 22 to 26 weeks is generally considered potentially viable. The uterine fundus is palpable at the umbilicus at 20 weeks. After 20 weeks, the gestational age of the fetus can be estimated by measuring the fundus from the pubic symphysis to the top of the fundus. The fundal height in centimeters corresponds roughly to the gestational age in weeks. Before approximately 22 to 24 weeks’ gestation, all efforts should focus on the mother, with no modifications to CPR.  Beyond 22 weeks or if the gravid uterus can be palpated above the umbilicus, several modifications of CPR should be instituted: (1) the patient should be positioned to minimize aortocaval compression, and (2) appropriate preparations for a potential cesarean section and care of a viable fetus should be made.

Limitation of aortocaval compression is achieved by (1) having someone manually displace the uterus to the left, (2) tilting the patient 15 to 30 degrees on a tiltable table, or (3) placement of a roll or a Cardiff wedge, if available, under the patient’s right hip and flank. The Cardiff wedge provides a tilt of 27%, allowing 80% of the compressive force, compared with CPR in the supine position, which maintains 30% or less of normal cardiac output in nonpregnant adults.  The “human wedge” has been advocated for bystander CPR. In this technique, the patient lies across the thighs of the rescuer, who is in a kneeling position. Despite relatively clear current recommendations regarding resuscitation in pregnancy, there is little research in this area.

Massive fetomaternal transplacental hemorrhage causes alloimunization in Rh incompatibility but also endangers the fetus by severe fetal anemia and resulting fetal distress and possible exsanguination. ABO incompatibility causes less severe disease.

The Kleihauer-Betke test identifies fetal cells in a maternal blood sample. Most laboratories screen for FMH of 5 mL or more. Unfortunately, the amount of FMH sufficient to sensitize most Rh-negative women is well below this 5-mL sensitivity level. Therefore, all Rh-negative mothers who have a history of abdominal trauma should receive one prophylactic dose of Rhesus immune globulin (RhIG). In the first trimester, one 50-g dose is used because total fetal blood volume is only 4.2 mL by 12 weeks’ gestation and a 50-g dose covers 5 mL of bleeding. During the second and third trimesters, a 300-?g dose of RhIG is given, which protects against 30 mL of FMH. Beyond 16 weeks’ gestation, the total fetal blood volume reaches 30 mL, so it is quite possible that massive FMH may exceed the efficacy of one 300-g dose of RhIG. Therefore, it is unlikely that a Kleihauer-Betke test is useful in the treatment of severely injured pregnant trauma patients.

References:

Rosen’s Emergency Medicine. 7^th editon. Pages 252-261.

Tintinelli’s Emergency Medicine.  7^th edition.

Case Presentation by Dr. Ayse Avcioglu

CC: Bleeding from tracheostomy

HPI: A 48 year old male presents from a long-term care facility for bleeding from his tracheostomy tube.  Per nursing staff, about 10-20 cc’s of bright red bloody secretions were noted emanating from the tube which ceased spontaneously.  Information was obtained from transfer records as patient could not provide information because he had recently suffered anoxic brain injury.  Subsequently a surgical tracheostomy was performed 11 days ago.  There is no history of fever, increased sputum production, night sweats or weight loss.

ROS:  negative except for HPI

PMH: Diabetes, seizure disorder, hypertension, gunshot wound to chest

PSH:  Tracheostomy, gastrostomy tube

Meds:  Amlodipine, insulin, lorazapam, phenytoin, rosuvastatin, aspirin,

clonidine, isosorbide dinitrate, hydralazine

Allergies:  NKDA

SH:  history of polysubstance abuse including alcohol and cocaine.

FH:  diabetes, chronic kidney disease

Physical Exam

VS:  BP:  180/86 mmHg, P: 75, RR: 24 T: 36.0 C, Pulse ox: 95% on room air

General: eyes open, no acute respiratory distress

HEENT:  NC/AT, PERRL, borderline pallor, anicteric

Neck:  supple.  Tracheostomy tube with blood tinged sputum.  Gauze saturated in blood.  Minimal blood around stoma.

CVS:  normal S1/S2, no murmurs, rubs or gallops.

Lung:  scattered rhonchi 

GI:  abdomen soft, nontender, nondistended.  Peg-tube in place.

 Musculoskeletal: limbs atraumatic, nontender to palpation. Some atrophy of leg muscles.

 Neuro:  eyes open.  Does not verbalize, withdraws to pain.

 Skin: warm, dry, no decubitus ulcers, no petechiae

Questions: 

1.  Given the time frame of the tracheostomy stoma creation, what is the most likely cause of bleeding?

A.  Bronchopneumonia

B.  Erosions secondary to tracheal suction

C.  Granulation tissue

D.  Tracheo-innominate artery fistula

2.  What would be the next step in management?

A.  Admit to the medical intensive care unit.

B.  Attempt to suction trachea.

C.  Obtain surgical consultation in the emergency department.

D.  Place on humidified oxygen, observe for two hours, discharge if no

further bleeding occurs.

3. While examining the patient, a sudden massive gush of blood is noted from the tracheostomy and patient becomes hypoxic.  What is the FIRST step in management?

A.  Apply digital pressure through tracheal stoma and wheel patient to operating room

B.  Call blood bank for immediate 2 units of O negative blood

C.  Obtain stat surgery consultation for operative repair

D.  Overinflate tracheostomy cuff

Discussion

1.  The answer is D.  Bleeding around the stoma or hemoptysis in any patient with a tracheostomy should be fully investigated.  The differential diagnosis of the cause of bleeding is based on the lag time between tracheostomy creation and subsequent bleeding.   Tracheo-innominate artery fistula is a rare life-threatening complication of tracheostomy.  It usually results from direct pressure from the tracheal cannula against the innominate artery, or from a cuff that is overinflated.   The peak incidence of presentation is between the first and second week.  About 50% of patients have a sentinel bleed which may be mild and should not be ignored because of the potential for sudden massive hemorrhage.  (B, C) Hemorrhage occurring within 48 hours is usually associated with local factors such as puncture of anterior jugular or inferior thyroid veins, granulation tissue, erosions due to suction or coagulopathy.  A. Bronchopneumonia would be more likely if the patient had a history of fever and increased purulent secretions.

2.  The answer is C.    When tracheo-innominate artery fistula is suspected, the patient must be evaluated by a surgeon in the emergency department and transported to the operating room for fiberoptic bronchoscopy with definitive surgical repair. A.  The patient should ideally be admitted to a surgical services team who are familiar with the management of this complication as a delay in diagnosis may result in death through asphyxiation. B. If the bleeding has stopped and the airway is clear, it is best not to disturb clots in the trachea by suctioning or movement of the tracheostomy tube in order to prevent increased rate of hemorrhage.  D.  Observation followed by discharge would be inappropriate without further assessment of the source of bleeding. Consider more than 10 mL of blood to be arterial.

3.  The answer is D.  The first step would be to hyperinflate the tracheal cuff in an attempt to compress the artery against the sternal wall.  This maneuver alone is successful in 85% of cases.

If this attempt fails, insert an endotracheal tube through oropharynx, remove tracheostomy tube and position the endotracheal tube cuff distal to bleeding site to protect airway.  B. Calling the blood bank for blood transfusion may become necessary if bleeding continues, but airway management takes priority.   C. Notifying the surgeon will become critical but is not the first step in management.  A. If initial attempts to control bleeding are unsuccessful, insert index finger through stoma, compressing the trachea against the sternum. This is the most reliable technique to stop the bleeding.  Hold continued pressure while simultaneously wheeling the patient to operating room.

References:

Roberts and Hedges Clinical Procedures in Emergency Medicine.  5^th ed.  Pages 124-137.

Tintinalli’s Emergency Medicine. 7^th ed. Pages 1592-1595.

Grant, C.A.  Tracheo-innominate artery fistula after percutaneous tracheostomy: three case reports and a clinical review.  British Journal of Anesthesia 96 (1): 127–31 (2006).

Case Presentation by Dr. Debia Kim

CC: “My eyes are blurry”

HPI:  31 y/o M reports 2 weeks of worsening headaches and 2 days of double vision after being hit in the back of the head with a metal napkin ring holder by his fiancee.  Since being hit in the head, he has been having intermittent, occipital, throbbing headaches which are partially alleviated by Motrin.  In addition to the headaches, he began experiencing double vision that began a day ago.  He tried to “sleep it off,” but on waking today he was still seeing double.  He denies pain in his eyes, denies red eyes, denies discharge, denies any new medications.  He states that when he closes one eye, the double vision does go away.  He can’t say which eye is worse.  He does not wear contacts or glasses, does not use eye drops.   Denies any numbness or tingling in his face, denies trouble with chewing, swallowing, or moving his facial muscles.  Denies change in hearing.  States he can walk “just fine” but prefers not to write and drive because of the blurry vision.  Denies nausea, vomiting, fever, neck ache, sick contacts.

REVIEW OF SYSTEMS: EYES:  Positive for double vision.  Negative for eye pain.  Negative for decreased vision.  Negative for photophobia. ENT: Negative for neck pain. GASTROINTESTINAL:  Positive for nausea, but negative for vomiting. MUSCULOSKELETAL:  No pain elsewhere in his body.  No trauma anywhere else in his body from the altercation with his girlfriend. NEUROLOGIC:  Positive for throbbing headache that waxes and wanes.

PAST MEDICAL, FAMILY, AND(OR) SOCIAL HISTORY:

PAST MEDICAL HISTORY:  None.

PAST SURGICAL HISTORY:  None.

MEDICATIONS:  Motrin p.r.n. ALLERGIES:  NONE.

SOCIAL HISTORY:  Daily smoking, occasional ethanol, occasional marijuana, but he did not report any use of ethanol or drugs within the last few days.  He is currently unemployed.

PRIMARY CARE PHYSICIAN:  None.

EXAMINATION OF ORGAN SYSTEMS-BODY AREAS:

VITAL SIGNS:  Blood pressure 131/70, heart rate 65, respirations 16, temperature 36.6, and pulse ox is 97% on room air. CONSTITUTIONAL:  This is a well-nourished, adult gentleman, in no acute cardiopulmonary distress, sitting calmly on the stretcher.

HEENT:  Head is normocephalic and atraumatic.  Nontender over the face and scalp.  The patient has a slight right ptosis, but his facies are otherwise symmetric.  He has anisocoria with right pupil that is enlarged nearly 8 mm.  The left pupil that is normal about 4.  Both pupils are reactive with no afferent defect.  His vision is 20/100 in the right eye and 20/20 in the left.  He does have some binocular double vision; however, when each eye is covered independently, he has monocular vision restored.  His extraocular movements are restricted.  His right eye cannot abduct completely to the right and he has trouble looking up; however, he is able to look down and to the left without difficulty on my examination.  Funduscopic exam is incomplete, but normal vasculature is visualized in both eyes.  The optic disks are incompletely visualized.  Sensation to light touch in the face is symmetric.  The patient is nontender over the bony prominences of his face.  Posterior pharynx is clear.

NECK:  Throat supple.  Trachea midline with no meningismus.

CARDIOVASCULAR:  Regular rate and rhythm.  Positive S1 and S2.  No tachycardia. LUNGS:  Clear bilaterally.

ABDOMEN:  Soft, flat, nondistended, and nontender.

MUSCULOSKELETAL:  Nontender over the arms and legs.

SKIN:  Warm and dry.

NEUROLOGIC:  Alert and oriented.  Speech fluent and appropriate.  Sensation to light touch intact over his facies symmetrically.  He can demonstrate a symmetric smile.  Midline tongue on protrusion.  He can lift his eyebrows and close his eyes.  He can shrug against resistance.  He can puff out his cheeks.  He demonstrates symmetric grip strength with normal finger-to-nose.  He has a normal gait and balance when walking through the emergency department.

QUESTIONS:

1)  Which cranial nerve(s) is(are) affected?

2)  What is the patient’s most likely diagnosis?

a) Bell’s Palsy

b) Multiple Sclerosis

c) PCA Aneurysm

d) Horner Syndrome

e) Brain bleed!

3)  Which imaging study would best provide a diagnosis?

ANSWERS:

1)  CN III palsy

2)  C – PCA Aneurysm

3)  MRI/MRA brain

DISCUSSION:

Neuro-ophthalmologic diagnoses are often challenging to sort out.  In this young patient with headache, a CN III palsy with ipsilateral pupillary dilatation is a posterior communicating artery aneurysm until proven otherwise.

PCOM aneurysms are the second most common Circle of Willis aneurysms (the first being ACOM).  PCOM aneurysms arise from the internal carotid artery near the PCOM origin.  Expansion here causes compression of the outer fibers of CN III as it travels out of the brain– which cause the nerve palsy and pupillary dilatation.

New onset diplopia is the most common presentation of CN III and VI palsies.  It can be painful or painless.  EOM testing will be abnormal with lateral gaze preserved in pure CN III palsy (unlike CN VI palsy, which will have abnormal lateral gaze with worsening diplopia on the affected side).  This patient presents with mixed EOM findings.  He also has decreased visual acuity in the R eye, which was thought to be secondary to his pupillary constriction problems (can’t focus) rather than an additional CN I issue.  This patient’s upward and medial gaze is preserved, which points away from a stroke or a demyelinating disease (such as multiple sclerosis) causing intranuclear ophthalmoplegia from lesion of the medial longitudinal fasciculus.  CN VII palsy (such as Bell’s palsy) can also present with ptosis but will classically be associated with problems of facial expression — it should not cause anisocoria or EOM issues.  Lastly, Horner syndrome also presents with ptosis and pupillary abnormalities.  In a Horner syndrome, the problem is interruption of the sympathetic inputs to the eye.  The classic physical findings would be ipsilateral ptosis, miosis (rather than dilatation as in our patient), and anhydrosis in a patient with a history of zoster, tumor, or trauma (to the ipsiliateral neck where the sympathetic plexus surrounds the carotid artery).  Lastly, this is a young nondiabetic and nonhypertensive patient.  Patients who do have such vasculopathies (diabetics especially) can develop acute CN III palsy due to vascular compromise of the nerve.  In vascular compromise of CN III, the central nerve fibers are most often infarcted first, which will cause a nerve palsy with pupillary sparing (EOM problems WITHOUT anisocoria).

The best imaging choice to diagnose a posterior circulation abnormality such as aneurysm is an MRI/MRA of the brain.  Given the broad differential for neuro-ophthalmologic emergencies and history of (relatively) recent trauma in our patient, a non-contrast head CT was the first test performed to rule out the possibility of an already bleeding significant aneurysm.  MRA of the neck was also done to assess the carotids and evaluate for Horner syndrome.  Neurosurgery, neurology, and ophthalmology services were consulted.  Blood pressure control was strictly monitored.

The patient underwent emergent coiling of the aneurysm, did well, recovered, and was discharged home.  He and his fiancee have cancelled their wedding plans.