COLA 11 (2014-2016) - Michigan College of Emergency Physicians

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COLA 11

(2014-2016)

HEATHER CRONOVICH, DO

JENNIFER STEVENSON, DO

Urologic Trauma Guidelines: a 21st Century Update

CME article through Medscape

Primarily intended for surgeons

The genitourinary system is involved in about 10% of all traumatic injuries, kidney being most commonly injured

Important to get the history of a solitary kidney if possible

Suggested Readings for

COLA 2014 - 2016

Urologic Trauma Guidelines: a 21st

Century Update http://www.medscape.org/viewarticle/7

27952 09/10

Position paper update: gastric lavage for gastrointestinal decontamination

Clinical Toxicology (2013), 51 140-146

Transfusion Medicine for Trauma Patients:

An Update www.medscape.org/viewarticle/749747

9/23/11

Prehospital Triage to Primary Stroke Centers and Rate of Stroke Thrombolysis http://archneur.jamanetwork.com/article.as

px?articleid=1704352

JAMA Neurol.

2013; 70(9): 1126-1132

Penicillin to Prevent Recurrent Leg

Cellulitis

NEJM 2013 368 (18): 1695-1703

Emerging Battery-Ingestion Hazard:

Clinical Implications http://pediatrics.aappublications.org/co ntent/125/6/1168.long 05/10

Hidradenitis Suppurativa

NEJM 2012; 366: 158-164 1/12/12

Herpes Zoster

NEJM 2013; 369: 255-263 7/18/13

Introduction to the Guidelines for the

Management of Acute Cervical Spine and Spinal Cord Injuries.

journals.lww.com/neurosurgery/toc/2013

/03002

March 2013

The Current Understanding of Stevens-

Johnson Syndrome and Toxic Epidermal

Necrolysis www.medscape.org/viewarticle/751622 10/

21/11

Be Prepared—The Boston Marathon and

Mass Casualty Events

NEJM 2013; 368: 1958-1960

Immediate and Delayed Traumatic

Intracranial Hemorrhage in Patients with

Head Trauma and Preinjury Warfarin or

Clopidogrel Use

Ann Em Med 59: 6: 460-468 June 2012

1/19/2015

Renal Trauma

Deceleration injuries can be devastating

Renal artery thrombus

Renal vein disruption

Renal pedicle avulsion

Seatbelts, steering wheels and airbags can compress the renal artery between the abdominal wall and spine leading to thrombus

Renal injury

Hemodynamic stability guides management

Hematuria is a hallmark of renal trauma but not always present nor correlate with degree of injury

IV contrasted CT scan is the gold standard for diagnosis of renal injury

CT angiography help assess the renal vasculature

Renal Injury

Blunt, non deceleration trauma, microscopic hematuria, no shock – imaging can be withheld

Any degree of shock – CT imaging is indicated

Rapid deceleration trauma, penetrating injury to the region of the kidneys – CT imaging is indicated

IVP is no longer the preferred imaging modality

1

Renal Artery Avulsion Renal Injury Management

Absolute indications for surgery

Life-threatening renal hemorrhage

Expanding or pulsatile peri-renal hematoma

Relative indication for surgery

Persistent bleeding

Suspected renal pelvis injury

Suspected ureteral injury

Conservative management is the treatment of choice for most patients

Renal Injury Management

Penetrating renal trauma

Recommend conservative treatment unless the injury involves the hilum, continued bleeding, ureteral or pelvic laceration

Follow CT as indicated but not routine

Fever, increased pain, persistent bleeding

Renal Injury Complications

Delayed retroperitoneal bleeding can occur within several weeks of the injury

Selective angiographic embolization

Perinephric abscess

Percutaneous drain

Hypertension

Delayed inset of hematuria

AV fistula

1/19/2015

Ureteral Trauma

Most commonly iatrogenic

No classic symptoms or signs

Hematuria only present in 50%

CT is most frequently used diagnostic modality

Consider KUB 30 minutes after IV contrast if diagnosis is still in question

Treated with stents, nephrostomy tubes, surgeon stuff…

Bladder Trauma

Blunt trauma results in the majority of bladder injuries

High association with pelvic injuries

Full vs. empty bladder

2

Bladder Trauma

Most common symptoms are gross hematuria and abdominal pain

Suprapubic bruising, abdominal distention, voiding problems

Combination of pelvic fracture and gross hematuria strongly suggests bladder rupture

Indication for immediate cystography

Retrograde cystography

Makes the diagnosis 85-100% of the time

Blunt Urethral Trauma

Blood at the meatus/vaginal introitus

Diagnostic modality of choice is the retrograde urethrography

Authors recommend making a single attempt to pass a foley catheter in the event of urethral injury

If unsuccessful, urology needs to work their magic

1/19/2015

Open Anterior Male

Urethral Injuries

Require immediate surgical exploration

You don’t even want to know what they do here…

Blunt Scrotal Trauma

Can lead to testicular rupture or dislocation

Ultrasonography is recommended

Exploration is recommended in the event of equivocal ultrasound findings

Vulvar Trauma

Can result in difficulty voiding

Consider CT scan of the pelvis

Most do not require surgery

NSAIDS, ice packs

Consider further exploration under anesthesia if necessary

Penetrating Penile Trauma

Animal and human bites are associated with a high risk of infection

Consider appropriate antibiotics for 10-14 days

Rabies

Surgical exploration if Buck’s fascia penetrated

3

Transfusion Medicine for

Trauma Patients: An Update

Murthi et al.

Expert Review of Hematology. 2011;4(5):527-537

Introduction

Injury is still the most common cause of death in young people

Traumatic injury

 leads approx. 9% of the population to seek medical care each year

Consumes 5% of all medical costs

Uses about 7% of the blood supply

Massive bleeding patients die quickly and trauma transfusion services must be able to respond to the special physiologic & logistic needs of these patients

1/19/2015

Introduction

In 2008, authors reviewed the practical interface between transfusion medicine and the surgery and critical care of severely injured patients 1

Epidemiology of injury

Organization and extent of trauma systems

Blood use in trauma resuscitation and subsequent care

Complications of blood use

How new technology was changing thoughts about the treatment & control of hemorrhage and the need for blood products

Introduction

This article examines new thinking & evidence of the most rapidly evolving issues

The coagulopathy of trauma

Damage control resuscitation

Advances in monitoring

Evolving issues in blood safety

The Coagulopathy of

Trauma

Direct loss and consumption of coagulation factors, dilution, hypothermia, acidosis and fibrinolysis all diminish hemostasis

 Can occur independently, but all occur more frequently and severely with worsening degrees of injury

 Interaction can drive the coagulation system beyond function and recuperative limits

Acute Coagulopathy of Trauma &

Shock

The Coagulopathy of Trauma:

Hemorrhage

Blood loss is often a presenting symptom of injury, but can be masked by internal bleeding or evacuation at site of injury

Patients in stage IV shock may have lost up to 40% of their blood volume

Proportional loss of coagulation factors and platelets

4

The Coagulopathy of

Trauma: Dilution

Physiologic hemodilution via vascular refill

 Loss of hydrodynamic bp leaves the colloid osmotic activity of plasma unopposed & water moves back into the intravascular space

 Diluting plasma proteins

 moves into the vascular space to dilute the plasma proteins

Each protein is diluted equivalently and their interactions (such as the assembly of factors IXa,

VIIIa, and X on platelet surfaces) is reduced in proportion to the product of the individual reductions in factor concentration

A 37% loss in the individual factor concentrations combines to cause a 75% reduction in overall complex activity

Iatrogenic dilution (with crystalloids or colloids) has similar effect

The Coagulopathy of Trauma:

Hypothermia

Hypothermia contributes to the coagulopathy of trauma by reducing platelet activation

Plasma coagulation factor enzyme activity decreased by ~5% with each 1°C fall in temperature

 Anticoagulant activity also decreases

Platelet activation by the von Willebrand factorglycoprotein Ib (IX, V) interaction is profoundly cold sensitive

This interaction is absent in 75% of individuals at

30°C and is compromised severely enough at

32°C that survival f severely injured hypothermic individuals is rare

The Coagulopathy of

Trauma: Acidosis

Acidosis is common in shock & profoundly affects the plasma coagulation system

A coagulation factor complex with normal activity at pH 7.4 has 50% of normal activity at pH

7.2, 30% at pH 7.0, 20% at pH 6.8

The Coagulopathy of Trauma:

Factor consumption

Conventional view: coagulation factor substrates are consumed in clotting, but the associated enzymes are not

However, in high-energy-transfer injury there are millions of endothelial microtears

Each of the factors are continuously activated and consumed

Releases tissue factor, phospholipids, histones and RNA

 All bind or activate coagulation factors

The Coagulopathy of Trauma:

Factor consumption

Once activated

Factors VIIa and Xa are inactivated by tissue factor pathway inhibitor

Factors IIa, IXa, Xa, XIa and XIIa are irreversibly bound and cleared by antithrombin

Factors Va and VIIIa are inactivated by protein C

The more severe the injury, the greater the degree of both activation and consumption

The Coagulopathy of Trauma:

Fibrinolysis

Normally, clots are made and are stable for a period of time that allows control of bleeding and wound healing

High concentrations of thrombin lay down thick bundles of fibrin, activate the thrombin-activated fibrinolysis inhibitor, and activate plasminogen activator inhibitor, slowing the activation of plasmin

When the thrombin burst is weak, the thrombin-activated fibrinolysis inhibitor is not activated

When thrombin diffuses beyond the limits of the many endothelial microtears and encounters thrombomodulin on the surface of adjacent healthy endothelial cells, protein C is activated which in turn inactivated plasminogen activator inhibitor

With severe injury, the balance between the extent of injury and the capacity of the coagulation system to modulate fibrinolysis can be exceeded

1/19/2015

5

The Coagulopathy of

Trauma

Sum of all these disturbances

As blood becomes more dilute, cold and acidotic, activation slows and concentration-dependant regulation is lost

Begins when coagulation factor activities fall below

50% and is severe when they are <20% injury moderate injury severe injury

Rate of coagulopathic injury*

1%

10% severe injury and hypotension requiring resuscitation severe injury and hypothermia

40%

50% severe injury and 60% acidosis transfused trauma patient: hypothermia and acidosis revisited. J. Trauma

When all of the above are present

98%

Resuscitation With Red

Cells in Additive Solution

All of the effects were exacerbated by the shift from resuscitation with anticoagulated whole blood, which contained normal amounts of plasma, to the use of red cells in additive solution with only 35ml of plasma in each unit

The Acute Coagulopathy of Trauma & Shock

Brohi et al. (2003): 1,000 helicoptered trauma patients (London)

 The higher the injury severity score, the greater the incidence of coagulopathy, and the presence of coagulopathy predicted a four-times higher mortality rate

 In 2008: “hypoperfusion induces systemic anticoagulation and hyperfibrinolysis”

MacLeod et al. (2003): 20,000 Miami trauma center admissions

28% with prolonged PT: 35% increased risk of hospital death

8% with prolonged PTT: 426% increased risk of death

Hess et al. (2009): 35,000 UMSTC admissions

Increasing injury severity predicted a stepwise increasing fraction of patient with increased PT on admission; rose to 45% of all patient with an ISS >45

 PTT less sensitive but more specific: PTT ratio >1.5 & ISS >25, mortality was 90%

Dutton et al. (2010): 35,000 UMSTC admissions

Of those who died of hemorrhage: ~50% within 2hours, 80% by 6h after admission

Damage Control Resuscitation

Como et al. (2004): UMSTC year 2000 blood product audit

Noted only 8% of admission received red cells and only 6% received plasma, but a total of 5219 units red cells and 5226 units of plasma given

 Suggests they were worsening coagulopathy by early resuscitation with crystalloid and red cells in additive solution, then attempting rescue later with plasma & platelets

Began giving plasma sooner and in more balanced proportion to red cells

Consensus: resuscitation after massive hemorrhage should dramatically reduce dependence on crystalloid and focus on repletion of both red cells and plasma in 1:1 proportions

1:1

1/19/2015

Damage Control

Resuscitation: platelets

While most of the emphasis has been on the plasmato-red-cell ration, giving platelets can also be important

Increased use appeared to improve outcome

(Cosgriff et al. 1997)

Low admission platelet counts were strongly associated with mortality

(Hess et al. 2009)

Giving more platelets early is associated with lower mortality

(Holcomb et al. 2008)

Suggested that most of the benefit occurs in patients with brain injury

(Spinella et al. 2011)

Resistance to Damage

Control Resuscitation

Essentially 3 arguments:

1:1 plasma to red cell resuscitation is unproven largely unnecessary ratios are wrong

6

Survivor bias in

Baghdad study overestimated the size of the survival benefit of plasma treatment

1:1 plasma to red cell resuscitation is unproven ratios are wrong largely unnecessary

Giving 1:1 :1 addresses all blood component needs and is easy to administer in an emergency

ABC: Assessment of

Blood Consumption

1. penetrating mechanism?

2. SBP ≤90mmHg?

3. HR ≥120?

4. Positive FAST?

The Future of Resuscitation

Single- donor freeze dried plasma

Plasma-derived coagulation factor concentrates

TXA (tranexamic acid)

Fibrin bandages

Advances in patient monitoring

Blood Safety

 Most common causes of death from transfusion in the developed world are the immune and inflammatory complications of allogenic transfusion

Acute lung injury is the leading cause of transfusionrelated death

Key Issues

Traumatic injuries are the leading cause of death in young people

Coagulopathy in trauma is multifactorial

Standard of care: damage control resuscitation with red blood cells, plasma and platelet units given in equal numbers(1:1:1)

Resuscitation with plasma-derived coagulation factor concentrates is developing rapidly and will replace damage control resuscitation

Once hemorrhage control is obtained, lower transfusion triggers are desirable

Communication between transfusion and trauma services remains critical

1/19/2015

Penicillin to Prevent

Recurrent Leg Cellulitis

New England Journal of Medicine, 2013

Most cases of lower extremity cellulitis are due to

Group A Streptococcus

Recurrent infections lead to further damage to lymphatics and increased incidence of recurrence as well as increased morbidity and mortality

Penicillin to Prevent

Recurrent Leg Cellulitis

Prophylactic Antibiotics for the Treatment of

Cellulitis at Home I (PATCH I)

Effectiveness of a 12-month course of low dose penicillin on the rate of recurrence of lower extremity cellulitis in patients with a history of recurrent disease

7

Methods

Double-blinded, randomized, controlled trial

Compared 12 months of prophylactic penicillin with placebo

250 mg penicillin twice each day

Phoned participants for pill counts every 3 months

Recorded their level of compliance

Participants were monitored for reoccurrence for up to 36 months

There was no commercial support for this study

Participants

Recruitment occurred at 28 hospitals in the United

Kingdom and Ireland

Between July 2006 and January 2010

Patients with a recurrent episode of lower extremity cellulitis within the previous 24 weeks were eligible

Local warmth, tenderness, acute pain, unilateral/bilateral erythema, unilateral edema

1/19/2015

Primary Outcome

Time from randomization to the next medically confirmed episode of cellulitis

Secondary Outcomes

Proportion of participants with a repeat episode of cellulitis during the prophylaxis phase and during the follow up phase

Number of repeat episodes of cellulitis

Proportion of participants with new edema or ulceration during the prophylaxis phase and follow up phase

Number of nights in the hospital for cellulitis

Number of adverse reactions/events of interest

Cost effectiveness

Results

Randomized 136 patients to receive penicillin and

138 to receive placebo

Of the 274 enrolled, 247 underwent al least 18 months of follow up

78% reported taking at least 75% of the study tablets

Primary Outcome

Median time to first recurrence was 626 days in the penicillin group and 532 days in the placebo group

During the prophylaxis phase:

30 of 136 (22%) of those in the penicillin group had a recurrence

51 if 138 (37%)of those in the placebo group had a recurrence

Participants on penicillin group had a 45% reduction in risk of repeat episode of cellulitis compared to placebo

NNT to prevent one repeat episode in 5

8

Secondary Outcomes

Overall, participants in the penicillin group had fewer repeat episodes than placebo

119 versus 164, P = 0.02

During the prophylaxis phase, there were fewer recurrences in the penicillin group (76) as compared to the placebo group (122), P = 0.03

No significant difference was seen during the follow up phase

43 in penicillin versus 42 in placebo

Secondary Outcomes

No significant difference in development of edema or ulceration in either group during either phase there were 37 adverse events in the penicillin group and 48n in the placebo group

11 participants died but none were thought to be a result of the study medication

1/19/2015

Secondary Outcomes

Factors associated with a poor response to treatment include

Body-mass index of 33 or higher

Three or more episodes of cellulitis

Presence of edema

There was no significant difference in the use of health cares services or dollars between groups

Discussion

Low dose prophylaxis with penicillin given for a 12 month period almost halved the risk of recurrence during the intervention phase

Patients who receive prophylaxis had fewer recurrences over the subsequent three years, advantage seems to be lost after 3 years

Patients with a BMI of 33 or higher, multiple previous episodes, or lymphedema of the leg have reduced likelihood of response to the prophylaxis

Discussion

Perhaps a higher dose would be more successful in patients with a higher BMI

Perhaps a longer treatment duration would be of some benefit

Earlier studies suggest that a 6 months treatment protocol did not afford it’s participants any benefit

Emerging Battery-Ingestion

Hazard: Clinical Implications

Litovitz et al.

Pediatrics 2010;125;1168; originally published online May 24, 2010; DOI:10.1542/peds.2009-3037

2010

9

Objectives

Recent case studies suggest that severe and fatal button battery (aka button cell) ingestions are increasing and current treatment may be inadequate

Objective of study

To identify battery ingestion outcome predictors & trends

Define the urgency of intervention

Refine treatment guidelines

Study

In 1992, analyzed 2,382 battery ingestion cases

Most were benign

No deaths

Only 2 (0.1%) major effects

Button batteries lodged in the esophagus posed the greatest risk, requiring prompt removal

<15-18mm diam generally passed through the gut uneventfully

Removal was rarely indicated for batteries beyond the esophagus

Recent cases suggested that the nature of battery ingestions has evolved prompting this study to reassess the clinical course of battery ingestions and to refine treatment guidelines

1/19/2015

Button Batteries

As more homes use small electronics, the risk of these batteries getting into the hands of infants and young children increases

Remote controls

Thermometers

Games and toys

Hearing aids

Calculators

Bathroom scales

Key fobs

Electronic jewelry

Cameras

 Holiday ornaments

Methods

Three data sources examined

National Poison Data System (NPDS)

56,535 cases from 1985-2009

National Battery Ingestion Hotline (NBIH)

8,648 cases from 1990-2008

All 13 fatal and 73 major outcome (lifethreatening or disabling) cases involving the esophagus or airway button battery lodgment reported in the literature or to the NBIH at anytime were obtained

Limitations

(supplemental information)

Poison-center reporting is voluntary; thus, many cases are not reported

NBIH and NPDS data are gathered during telephone consultations, often with parents or patients, with incomplete access to detailed medical information

These limitations were mitigated for serious cases, when possible, through extensive telephone follow-up, contact with both health professionals and parents, and review of endoscopy or operative reports

Results: NPDS

NPDS

68.1% occurred in children younger than 6 y/o

20.3% in children 6-19 y/o

Only clinically significant (moderate, major or fatal) in 1.3% of ingestions

BUT, percentage of cases with clinically sig outcomes increased 4.4-fold from the first 3 years

(1985-1987) to the last 3 years (2007-2009)

10

1/19/2015

Results: NBIH

During 18.25 year period, 8,161 button battery & 487 cylindrical cell ingestions reported

Confirmed in 81.9% of cases by radiograph, battery in stool or emesis, or endoscopic retrieval

Children <6: 62.5% of ingestions

Four battery sizes accounted for 95% of ingestions

11.6mm (55.1%), 7.8-7.9mm (30.6%), 20mm (6.4%),

5.8mm (3.0%)

Ingestion of large-diameter cells (≥ 20mm) increased

From 1% in 1990-1993 to 18% in 2008

Button battery chemistry (known 57.7% of the time)

41.7% manganese dioxide/alkaline, 31.8% zinc-air,

13.1% silver oxide

Lithium (9% overall): BUT 1.3% (1990-1993) to 24% in 2008

Results: NBIH: Outcome predictors

Most important predictors of outcome

Battery diameter (20-25mm)

Age <4

Ingestion of >1 battery

Chemical system was not included in the model because it is highly correlated with diameter

99.3% of 20-25mm cells were lithium and 82.5% of lithium cells were 20-25mm

87.8% of manganese dioxide cells were 9-14mm

All silver oxide cells were <15mm

 The outcome of ingestion of small lithium cells was no worse than the outcome of ingestions of other small button cells

Results: NBIH: Outcome predictors

Of 33 major outcomes or fatal cases with known diameter

31 (93.9%) involved button batteries ≥20mm

No clinically significant outcomes were observed with 15-

18mm cells

Lithium cells were more likely associated with clinically significant outcomes

Age was an important predictor of severity

All fatalities and 85% of major effects occurred in children <4 y/o

A major effect or death occurred in 12.6% of children <6 y/o and ingested 20-25mm batteries

Results: hearing aids

 Whole hearing aids containing batteries

221 ingestions

78.7% by age ≥60 y/o

 Effects

89.2% had no effect

4.1% minor effect

1 patient with concomitant medial problems had moderate effect

Overall, no major effects or death

Results: cylindrical cells

Outcome was unknown more than twice as often because of the nature of the ingestions

At least 43% were intentional, suicidal or associated with a neuropsychiatric disorder;

6% by incarcerated individuals

37.8% of ingestions involved multiple cells

Compared with 8.7% of button battery ingestions

Results: NBIH & Medical Literature: clinical issues and the urgency of removal

13 fatalities (1977-2009), 9 (69%) in the most recent 6 years (2004-

2009)

All occurred in 11 month old- 3 y/o children

Only 1 ingestion was witnessed

Diagnosis was missed by health care providers in 7 of the 13 deaths

Nonspecific presenting symptoms

Batteries were in the esophagus 10 hours- 2 weeks before removal or death

9 cases: exsanguination as a result of esophageal fistulas into major arteries

(7 aortoesophageal)

Delayed, unanticipated, uncontrolled massive bleeding occurred up to 18 days after battery removal

11

Results: major outcomes

Major or fatal ingestions

20mm lithium cells (92.1%)

Children <4 y/o (91.8%)

Of all the fatalities reported with button battery ingestion, the highest fatality rate was in those ages

0-4 years

Unwitnessed (56.2% )

19 (46.3%) of the unwitnessed ingestions were misdiagnosed compared with 1 witnessed (mistaken for a coin)

 Misdiagnosed

 nonspecific symptoms

 misidentified as EKG electrodes, external objects or coins

 above the view on XR

Results: Time to remove

Battery was lodged in the esophagus for just 2-2.5 hours in 3 major outcome cases

Caused severe burns, esophageal stenosis that required repeated dilatation, a tracheostomy for persistent stridor, or bilateral vocal cord paralysis

Estimated time to remove

Delayed removal followed failure to seek medical care promptly, misdiagnosis, failure to recognize need for urgent removal, transfer for pediatric endoscopy, or insistence on fasting before administering anesthesia

80

60

40

20

0

7

17

Time to remove

27

36

42

48

60

67

72

1

Results: Complications in major outcome cases

Tracheoesophageal fistulas (35 cases, 47.9%)

Other esophageal perforations (17 cases,

23.3%)

Esophageal strictures or stenosis usually requiring repeated dilations (28 cases, 38.4%)

Vocal cord paralysis from recurrent laryngeal nerve damage (7 cases, 9.6%)

Other: mediastinitis, cardiac or respiratory arrests, pneumothorax, pneumoperitoneum, tracheal stenosis or tracheomalacia, aspiration pneumonia, empyema, lung abscess, spondylodiscitis complications

9.60%

38.40%

47.90%

23.30% tracheoesophageal fistulas other esophageal perforations esophageal strictures or stenosis vocal cord paralysis

Results: Complications in major outcome cases

Tracheoesophageal fistulas

 Became symptomatic up to 9 days after battery removal

Esophageal strictures or stenosis

Delayed by weeks to months

The single case of spondylodiscitis

 presented nearly 6 weeks after battery removal

Many patients required a tracheostomy, feeding tube, repeated esophageal dilation, and/or surgical esophageal or tracheal repair

1/19/2015

Discussion

All 3 data sources signaled worsening outcomes for battery button ingestions

 paralleling the increase in household use and ingestion of 20mm lithium coin cells

Serious battery ingestion complications are related to local corrosive injury rather than systemic poisoning from battery contents

Discussion: Lithium

Lightest metal

Offers electrochemical efficiency, high-energy density, long selflife, and cold tolerance

Major injury mechanism:

 generation of an external current, electrolysis of tissue or mucosal fluids and local generation of hydroxide, rather than leakage

20-mm lithium cells are 3V cells (twice the 1.5V of other button cells), have a higher capacitance and generate more current

Lithium cells generate more hydroxide, more rapidly

12

Discussion

The external electrolytic current generates hydroxide at the negative pole, therefore the anatomic position and orientation of a battery lodged in the esophagus may predict the specific subsequent injury

The most severe burns, delayed perforations and fistulas are anticipated in the area adjacent to the lodged negative battery pole

 Injury continues for days to weeks after battery removal because of residual alkali or weakened tissues

“negative-narrow-necrotic”

The negative battery pole, identified as the narrow side on lateral XR, causes the most severe necrotic injury

Discussion: missed diagnosis

Missed battery lodged in esophagus in at least 27% of major outcomes and 54% of fatal cases

 because of nonspecific presentations

 especially in unwitnessed ingestions

Strategies to avoid missed diagnosis remains elusive

?

1/19/2015

Discussion: treatment & outcome

Window for injury-free removal: <2 hours

The most severe outcome with ingestion of button batteries of 20mm or greater occurs within 2 hours

Hemorrhage occurred in 12 of the 13 deaths

The most prominent cause of death from button batteries is artereoesophageal fistulas

Discussion: treatment & outcome

Although outcome is determined by battery diameter and chemistry, these parameters are initially unknown in >40% of cases

Attempt to compare with common items

Batteries that are penny or nickel sized should be assumed to be 20-mm lithium cells

Item Diameter

(mm)

Pencil eraser 6-7

Dime

Penny

Nickel

Quarter

18

19

21

24

Revised Triage &

Treatment Guidelines

Batteries in the esophagus must be removed within 2 hours

If in the stomach or beyond in an asymptomatic patient

 leave to pass spontaneously with stool inspection or possible repeat radiograph in 10-14 days to confirm passage

Exception: if a magnet is co-ingested= mandates prompt removal

Revised Triage &

Treatment Guidelines

Children <6 y/o and ingested ≥15-mm batteries should have another XR in 4 days (increased from prior 2-3 day recommendation) to confirm that the battery has moved beyond the stomach

If still there: endoscopic retrieval

Earlier retrieval if symptomatic

May indicate gastric ulceration or undetected previous esophageal lodgment

13

Revised Triage &

Treatment Guidelines

XR should be examined for the battery’s double-rim or halo effect on AP XR or step-off on the lateral view

To make sure the “coin” or “EKG electrode” is not really a battery

Endoscopic removal of esophageal batteries

 vs. blind retrieval

Essential to determine the extent of injury and anticipate complications

Avoid pushing the battery into the stomach

Ineffective, unconfirmed, & unnecessary interventions

(supplemental information)

Ipecac

Laxatives

Polyethylene glycol electrolyte solution

Metoclopramide

Determinations of blood or urine concentrations of mercury or other battery ingredients and chelation therapy

1/19/2015

Updated NIBH

Guidelines

www.poison.org/battery/guidelines.asp

Hidradenitis Suppurativa

Chronic, recurrent inflammatory disease that affects skin that bears apocrine glands

Generally develops after puberty, more commonly in women (3:1)

Manifests as painful, deep-seated, inflamed lesions, including nodules, sinus tracts, and abscesses

Flares often occur premenstrually, generally subside in 7-10 days if untreated

Conclusions

Serious and fatal button battery ingestions are occurring with increased frequency as a result of the emergence of the 20-mm lithium coin cell as a popular household battery

To improve outcomes

Consider the diagnosis particularly in unwitnessed ingestions

Accurately discern batteries from coins

Immediately remove batteries lodged in the esophagus because sever injury can occur in just 2 hours

Anticipate delayed complications (most frequent fatal complication: fistulization into an artery causing hemorrhage)

Hidradenitis Suppurativa

About 1/3 of patients report a family history of the disease, autosomal dominant

Cigarette smoking and obesity are recognized risk factors

Increased frequency associated with Crohn’s disease and arthritis

14

Hidradenitis Suppurativa

This diagnosis is made clinically , oftentimes misdiagnosed and mistreated for years

Oftentimes misdiagnosed as ‘common boils’ and treated with incision and drainage or antibiotics

The Hurley staging system is used to describes severity and guide treatment

Hurley Stage I

Localized disease

Single or multiple abscesses without sinus tracts or scarring

Consider topical clindamycin for 3 months

Clinical experience supports the use of intralesional injections of glucocorticoids

1/19/2015

Hurley Stage II

Recurrent abscesses, sinus tract formation and scarring

Often treated with oral antibiotics with antiinflammatory properties

Androgens have been used based on antidotal evidence

Hurley Stage III

Diffuse or nearly diffuse involvement of the affected region, multiple intra-connected tracts and abscess over the entire area

Systemic immunosuppressant agents

 cyclosporine

TNF-a inhibitors

Treatment

Surgery is considered for scarred lesions and

Stage III disease

Local I&D is discouraged as it leads to more scarring and reoccurrence is the norm

Laser therapy has shown promising results

Use of external-beam radiation therapy has been described but the risks likely outweigh the benefits

Interestingly, there have not been studies done regarding the effects of weight loss and smoking cessation on the progression/severity of disease

Herpes Zoster

Jeffrey I Cohen, M.D.

The New England Journal of

Medicine

N ENGL J MED 369;3

July 18, 2013

15

Case vignette

A 65-year-old man presents with a rash of 2 days’ duration over the right forehead with vesicles and pustules, a few lesions on the right side and tip of the nose, and slight blurring of vision in the right eye. The rash was preceded by tingling in the area and is now associated with aching pain. How should this patient be evaluated and treated?

The Clinical Problem: risks

Major risk factor: increasing age

Women > men

Whites > blacks

Family history of herpes zoster > no history

Increased risk of childhood herpes zoster if chickenpox in utero or early infancy

Increased risk in immunocompromised patients with impaired T-cell immunity

The Clinical Problem: VZV

& HZ

HZ is caused by a reactivation of latent VZV in cranial-nerve or dorsal-root ganglia

Spreads along the sensory nerve to the dermatome

More than 1 million cases each year in the US

Annual rate of 3 to 4 cases per 1,000 persons

Unvaccinated persons who live up to age 85 have a 505 risk of herpes zoster

Up to 3% of patients require hospitalization

The Clinical Problem: postherpectic neuralgia

Pain persisting after the rash has resolved

 ie: pain for 90+ days after rash onset

Develops in 10 to 50% of cases

Increased risk

 with age (50+)

 severe pain at the onset of HZ

 with a severe rash and a large number of lesions

Can last months to years

May be severe and interfere with sleep and ADLs

The Clinical Problem: complications

Various neurological complications have been reported

Bell’s palsy

Ramsay Hunt syndrome

Transverse myelitis

TIAs and stroke

Ophthalmologic complications in the trigeminal nerve V1 distribution

Keratitis, scleritis, uveitis, acute retinal necrosis

Immunocompromised patients

Disseminated skin disease, acute or progressive outer retinal necrosis, chronic herpes zoster with verrucous skin lesions, development of acyclovir-resistant VZV

Can involve multiple organs

 patients may present with hepatitis or pancreatitis several days before the rash appears

Symptoms: rash

Dermatomal and does not cross the midline

Consistent with reactivation from a single dorsalroot or cranial-nerve ganglion

Thoracic, trigeminal, lumbar, and cervical dermatomes are most frequent sites, although any area of the skin can be involved

Often preceded by tingling, itching, or pain for

2 to 3 days

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Symptoms: rash

Begins as macules and papules

Evolves into vesicles and then pustules

New lesions appear over 3 to 5 days, often with filling in of the dermatome despite antiviral treatment

Usually dries with crusting in 7 to 10 days

Immunocompromised patients may have disseminated rash with viremia & new lesions for up to 2 weeks

Pain varies

Paresthesia (burning & tingling), dysesthesia (altered or painful sensitivity to touch), allodynia (pain with nonpainful stimuli), or hyperesthesia (exaggerated or prolonged response to pain)

Pruritus is also common

Diagnosis

Most diagnosed clinically

Atypical rashes may require direct immunofluorescence assay for VZV antigen or

PCR assay for VZV DNA in cells from the base of the uprooted lesion

PCR sensitivity 95%, specificity 100%

Immunofluorescence sensitivity 82%, specificity 76%

Herpes simplex virus: condition most commonly mistaken for HZ

Treatment & Prevention:

Antiviral Therapy

Recommended for HZ in certain nonimmunocompromised patients and in all immunocompromised patients

Indications for Antiviral Treatment in

Patients with Herpes Zoster

Age ≥50 yr

Moderate or severe pain

Severe rash

Involvement of the face or eye

Other complications of herpes zoster

Immunocompromised state

In patients with herpes zoster, those most likely to benefit from antiviral therapy are those over 50 years of age and immunocompromise d patients

Antiviral Therapynonimmunocompromised

Medication

Acyclovir (Zovirax®)

Famciclovir (Famvir®)

Valacyclovir (Valtrex®)

Brivudin (Zostex®,

Dose

800mg po 5x/day x 5-7d

500mg po TID x 7d

1g po TID x 7d

125mg po qd x 7d

*not available in the US, not FDA approved

Effects observed in controlled trials

Reduced time to last new-lesion formation, loss of vesicles, full crusting, cessation of viral shedding, reduced severity of acute pain

Reduced time to last new-lesion formation, loss of vesicles, full crusting, cessation of viral shedding, cessation of pain

Reduced time to last new-lesion formation, loss of vesicles, full crusting, cessation of pain

Reduced time to last new-lesion formation, full crusting, cessation of pain

Side effects

Malaise

Headache, nausea

Headache, nausea

Headache, nausea

CI in pts receiving fluorouracil or other flouropyramidines

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Antiviral Therapyimmunocompromised

Medication

Acyclovir (Zovirax®)

Foscarnet (Foscavir®)* for acyclovir-resistant VZV

Dose

10mg/kg IV q8h x 7-10d

Effects observed in controlled trials

Reduced time to last newlesion formation, full crusting, cessation of viral shedding, reduced cutaneous dissemination, reduced visceral herpes zoster

40mg/kg IV q8h until lesions are healed

Not reported

*off-label, not FDA approved for this use

Side effects

Renal insufficiency

Renal insufficiency, hypokalemia, hypocalcemia, hypomagnesemia, hypophosphatemia, nausea, diarrhea, vomiting, anemia, granulocytopenia, headache

• For immunocompromised patients requiring hospitalization or patients with severe neurologic complications

Antiviral Therapy

Initiate within 72 hours of onset of rash and last for 7 days

If new lesions are still forming after 72 hours or complications are present, may also start

TID valcyclovir and famciclovir vs. 5x/day acyclovir

Higher and more consistent levels of antiviral drug activity in the blood

Some studies suggest better at reducing pain

More expensive

Hasten the resolution of lesions, reduce the formation of new lesions, reduce viral shedding, and decrease the severity of acute pain

Do not reduce the incidence of postherpetic neuralgia

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Treatment & Prevention:

Glucocorticoids

Use with antiviral regimen remains controversial

Not been shown to reduce the incidence of postherpectic neuralgia

Prednisone or prednisolone taper may reduce acute pain, improve performance of ADLs, accelerate early healing, reduce time to complete healing

Avoid in patients with HTN, DM, PUD, osteoporosis, elderly

Used for certain CNS complications: vasculopathy, Bell’s palsy

Acute Pain Associated with

Herpes Zoster

Mild pain

NSAIDs or acetaminophen

More severe pain

Opioids

More effective than gabapentin

Gabapentin

Effective?: Yes in 1 trial, no in another

Lidocaine patches

TCAs

Used when opioids were insufficient

Eye Disease Associated with Herpes Zoster

Lesions in the V1 distribution of the trigeminal nerve

(including lesions on the forehead and upper eyelid)

Lesions on the tip or side of the nose or

New visual symptoms

Ophthalmologist evaluation

Other treatments may be added:

• Mydriatric gtts

• Topical glucocorticoids

• Medications to reduce intraocular pressure

• Intravitreal antiviral therapy

Postherpetic Neuralgia

Medications in randomized trials shown to reduce pain

Topical lidocaine

Anticonvulsant agents

 Gabapentin, pregabalin

Opioids

TCAs

Nortriptyline

Capsaicin

Combination therapy has been more effective than single agent

Ie: gabapentin + nortriptyline, opiate + gabapentin

Even with treatment, many patients still do not have good relief

Prevention of Herpes

Zoster

A live attenuated herpes zoster vaccine is recommended by the Advisory Committee on

Immunization Practices for people ≥ 60 yr to prevent herpes zoster and its complications

FDA approved it for persons ≥ 50 yr (based on a 2012 clinical trial) age

50-59 yr

60-69 yr

≥ 70 yr

Efficacy in preventing herpes zoster

70%

64%

38%

Efficacy in preventing postherpectic neuralgia

Not addressed

66%

67%

Herpes zoster vaccination

Reduction in risk of herpes zoster was significant for at least 5 years after vaccination

 effectiveness declined over time

In vaccinated persons who still got herpes zoster, pain was shorter in duration and less severe

After ~3 years Can be given to persons with a history of herpes zoster

Contraindications

Hematologic cancer pts who are undergoing chemotherapy or whose disease is not in remission, T-cell immunodeficiency, those receiving high-dose immunosuppressive therapy

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Infection Control

Less contagious than varicella, but can still transmit VZV to susceptible persons

Use contact precautions and cover lesions if possible

Areas of Uncertainty

Improved therapies needed

 for pain and postherpetic neuralgia

 to prevent the development of postherpetic neuralgia

Studies needed

 determine patients at highest risk for postherpetic neuralgia

Vaccine uncertainty:

The safety and effectiveness in immunocompromised patients

Duration of induced immunity

Need for booster doses

Conclusions and

Recommendations

Older persons are at increased risk for pain & complications

Postherpetic neuralgia, ocular disease, motor neuropathy, CNS disease

In the vast majority, diagnosis is clinical

Antiviral therapy

Most beneficial for persons who have complications or who are at increased risk for complications

Older persons >50 y/o & immunocompromised

Initiate within 72 hours and last for 7 days

Valacyclovir or famciclovir is preferred over acyclovir

Reduced frequency of dosing and higher levels of antiviral drug activity

Vignette recommendations

A 65-year-old man presents with a rash of 2 days’ duration over the right forehead with vesicles and pustules, a few lesions on the right side and tip of the nose, and slight blurring of vision in the right eye. The rash was preceded by tingling in the area and is now associated with aching pain. How should this patient be evaluated and treated?

Oral antiviral therapy with valacyclovir or famciclovir

Medication for pain (combination therapy ie: opioid

+ gabapentin)

Referred to ophthalmologist

Avoid contact with persons who have not had varicella or the vaccine until his lesions have completely crusted

Recommend getting the vaccine in 3 years

Introduction to the Guidelines for the Management of Acute

Cervical Spine and Spinal

Cord Injuries

Neurosurgery 2013

112 evidence based recommendations comparing the most current research with that from a decade ago

Immobilization

Immobilization of trauma patients who are awake, alert, and are not intoxicated, who are without neck pain or tenderness, who do not have an abnormal motor or sensory examination and who do not have any significant associated injury that might detract from their general evaluation is not recommended – Level II

Spinal immobilization in patients with penetrating trauma is not recommended due to increased mortality from delayed resuscitation – Level III

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Radiologic Assessment:

Asymptomatic Patients

In the awake, asymptomatic patient who is without neck pain or tenderness, who has a normal neurological examination, is without an injury detracting from an accurate evaluation, and who is able to complete a functional range of motion examination; radiographic evaluation of the cervical spine is not recommended – Level I

Discontinuance of cervical immobilization for these patients is recommended without cervical spinal imaging - Level I

Radiologic Assessment:

Symptomatic Patient

In the awake, symptomatic patient, high-quality computed tomographic (CT) imaging of the cervical spine is recommended – Level I

If high-quality CT imaging is available, routine 3view cervical spine radiographs are not recommended – Level I

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Radiologic Assessment:

Obtunded/difficult Patient

High-quality CT scan is recommended as the initial imaging modality of choice

Consider x-rays only if CT is not available and obtain CT when available

Pharmacologic Agents

High dose steroids are not recommended for treatment of spinal cord injuries and may even be harmful – Level I

Administration of GM-1 ganglioside (Sygen) for the treatment of acute spinal cord injury is not recommended – Level I

Atlanto-Occipital

Dislocation

Traction is not recommended in the management of patients with AOD, and is associated with a

10% risk of neurological deterioration – Level I

Kind of Random…

The routine use of CT and MR imaging of trauma victims with ankylosing spondylitis is recommended, even after minor trauma - Level III

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Pediatric injuries

Cervical spine imaging is not recommended in children who are greater than 3 years of age and who have experienced trauma and who:

 are alert have no neurological deficit have no midline cervical tenderness have no painful distracting injury do not have unexplained hypotension and are not intoxicated

Pediatric Injuries

Cervical spine imaging is not recommended in children who and who

3 years of age who have experienced trauma

 have a GCS>13 have no neurological deficit have no midline cervical tenderness have no painful distracting injury are not intoxicated do not have unexplained hypotension and do not have motor vehicle collision (MVC) a fall from a height greater than 10 feet (?! – must be a typo) or non-accidental trauma (NAT) as a known or suspected mechanism of injury (?!)

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Pediatric Injuries

(SCIWORA)

In spinal cord injury without radiographic abnormality (SCIWORA) MRI of the region of suspected neurologic injury is recommended

Radiologic screening of the entire spine is recommended

Vertebral Artery Injury

Computed tomographic angiography (CTA) is recommended as a screening tool in selected patients after blunt cervical trauma who meet the modified Denver Screening Criteria for suspected vertebral artery injury

The Denver Screening

Criteria

Focal neurological deficit

Arterial hemorrhage

Cervical bruit in a patient less than 50 years of age

Expanding neck hematoma

Neurological exam inconsistent with head CT scan

Cerebrovascular accident on follow-up head CT not seen on initial head CT

The Denver screening criteria lists the following risk factors for blunt Cerebrovascular injury

Presence of Leforte II or III fractures

Cervical spine fractures involving subluxation

Cervical spine fractures involving C1-C3

Cervical spine fractures extending into the transverse foramina

Basilar skull fractures with carotid canal involvement

Diffuse axonal injury with a Glasgow Coma Scale of 6 or less

Near hanging injuries with anoxic brain injury

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Vertebral Artery Injury

Treatment

It is recommended that the choice of therapy for patients with vertebral artery injury, anticoagulation therapy versus antiplatelet therapy versus no treatment, be individualized based on the patient’s vertebral artery injury, their associated injuries and their risk of bleeding

The role of endovascular therapy has yet to be defined; therefore no recommendation regarding its use in the treatment of vertebral artery injury can be offered

Position Paper Update:

Gastric Lavage for

Gastrointestinal

Decontamination

Benson et al.

Clinical Toxicology (2013), 51 , 140-146

Introduction

Gastric lavage has been used as a treatment for poisoned patients for over 200 years

Concern that risks may outweigh benefit

1997 & 2004 Gastric Lavage Position Papers

 literature review by panel of experts: American Academy of

Clinical Toxicology (AACT) & the European Association of Poisons

Centres and Clinical Toxicologists (EAPCCT)

No conclusive evidence to support continued use

Consequences

Poison centers seldom recommend gastric lavage

Use in EDs has declined steadily

Reduced availability of equipment or expertise to perform gastric lavage

Animal studies:

summary of 2004 Position Paper

3 studies examined the utility of gastric lavage in reducing the bioavailability of various markers

 1 study: dogs given sodium salicylate then lavaged at 15 min or 1 hour

Mean portion of salicylate recovered: 38% (15min), 13% (1hr)

2 studies: barium sulfate used as a marker

 Mean recovered: 26% and 29% (30min), 13% and 8.6% (60min)

Another study compared lavage + activated charcoal vs. no treatment in a simulated asa overdose

Peak plasma concentrates reduced by 37% vs no treatment

Method

An expert panel of 9 members was appointed by the AACT & the EAPCCT to update the 2004

Gastric Lavage Position Paper

Systematic literature review from January 2003-

March 2011

683 articles

69 offered the possibility of applicable human data

Ultimately 15 contributed to this revision of the Position

Paper

Drafted and reviewed for comments. Final product is endorsed by the Boards of both the

AACT & EAPCCT

Animal studies:

new studies

No new studies since 2004

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Experimental studies in volunteers: summary of 2004 Position Paper

Limitation: doses used in mock overdoses are substantially lower than doses actually encountered in real overdoses

4 studies examined the utility of gastric lavage using simulated drug overdoses

Drugs: ampicillin (32% reduction at 1hr), aspirin (8% reduction at 1hr), 2 multi-drug studies of temazepam, verapamil, moclobemide (not significant at 30min)

3 studies examined the effect of lavage on recovery of markers instead of drugs

Markers: cyanocobalamin, Tc 99m (30% recovery at

19min), radiolabeled water (85% recovery at 5min)

Experimental studies in poisoned patients:

summary of 2004 Position Paper

Post-lavage endoscopy was used to evaluate the thoroughness of gastric decontamination in 17 patients (16-72 yr) and lavaged with 2.5-5.5L of tap water using a Faucher tube size 33

88% had solid debris still visible in the stomach

2 poisoned patient marker studies

1 used radiovisible polythene pellets: 20 ingested

5min before lavage (48% retrieval)

1 used a liquid 100-mg thiamine preparation (90% retrieval at 5min)

Experimental studies in volunteers: new studies

No new studies

Experimental studies in poisoned patients:

new studies

No new studies

Case reports:

summary of 2004 Position Paper

Continued drug absorption is known to occur after gastric lavage has been performed

Sharman et al. (1975) recovered drug hours after gastric lavage in 19 patients when hourly NG aspirates were obtained

Lavage can be ineffective when drug concretions form during overdose

Schwartz (1976) described a 56 y/o pt who developed a concretion after ingesting 36g of meprobamate

Victor et al. (1968) in an autopsy series described

2 cases of barbiturate poisonings in which residual drug was found despite lavage prior to death

Case reports:

new studies

Borras Blasco et al. (2005): 32 y/o man who ingested 50 sustained release lithium tablets

Continued rise in serum lithium concentrations over

22hrs despite treatment with lavage, WBI, and activated charcoal

Schwerk et al. (2009): 16 y/o girl who ingested 43 tablets of etilefrin; lavaged within 30min of ingestion with no success

Endoscopy revealed a pharmacobezoar. Tablets were removed. Authors recommended endoscopic tablet removal in pts who have failed to respond to lavage or activated charcoal

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Case reports:

new studies

3 case reports stressed the importance of lavage in unique situations in which the drug absorption might be delayed

Adler et al. (2011): 50y/o woman comatose & hypothermic. CT noted large number of tablets in her stomach.

 Gastric lavage to remove tablets and assist with rewarming efforts. Recovered fully in 3 days.

Kimura et al. (2008): 2 cases where CT was used to identify large numbers of tablets in the stomachs of pts presenting past a 1hr cut off point and where nasogastric lavage was use to retrieve tablet fragments

 aspiration pneumonia noted pills in gastric fundus. NGT lavage with 6L until clear, then activated charcoal given

Both patients recovered

No cases had gastric aspirates assayed so drug amounts could be quantitated

Unclear how important nonconventional lavage methods & ancillary treatments were in eventual recoveries

Clinical studies:

summary of 2004 Position Paper

A number of studies that have examined the utility of gastric lavage in specific types of overdose using the amount of drug recovered as a surrogate marker for treatment effectiveness

Barbiturates : recoveries have ranged from 0 to >450mg but virtually nonexistent after 4 hours

TCAs: mean 94mg at a mean of 2.5h after ingestion.

Salicylate: recoveries of >1000mg were obtained in 6 of 23 cases

Jimson weed: 8 o 14 had evidence of seeds in aspirate

Acetaminophen: plasma concentrations dropped by mean of

39% with lavage

Studies do not address the impact of lavage over time since the initial doses were unknown.

Did not examine the impact of lavage on clinical recovery

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Clinical studies:

summary of 2004 Position Paper

Others examined the value of gastric lavage on cohorts of overdose patients without restricting observations to a single agent

Comstock et al. (1981): reported lavage recovery rates – expressed as the percentage of patients in whom more than

10 therapeutic doses were recovered

Varied from 6% (short acting barbs) to 33% (amitriptyline); overall rate of 14%

Later prospective pseudo-randomized studies compared the frequency of clinical deterioration or improvement in patient treated with gastric lavage + activated charcoal vs. activated charcoal alone OR patients treated with lavage + activated charcoal vs. ipecac + activated charcoal

Lavage did not influence the clinical course

Clinical studies :

new studies

Li et al. (2009): literature review for strength of evidence for gastric lavage in organophosphorus pesticide poisoning

56 studies with positive results reported but Li et al. concluded that the observations needed to be replicated using higher quality methods before results could be accepted

Wang et al. (2004): examined the effect of gastric lavage on mortality rates with tetramine (rodenticide causing seizures) poisoning in China

Lower fatality rate vs pts not lavaged, even with severe intoxication. Concluded that lavage was an effective treatment. However, it was a retrospective review, so likely many uncontrolled variables

Clinical studies :

new studies

Amigό et al. (2004): prospective cohort trial comparing outcomes of pts treated with a GI decontamination algorithm vs. not

Algorithm allocated pts to treatment with ipecac, gastric lavage, gastric lavage + activated charcoal, activated charcoal alone, or no decontamination based on clinical condition, agent ingested and time since exposure

Less clinical deterioration in the group managed with the algorithm

Only 8 patients (of 94) were treated with gastric lavage alone, so role was unclear

Contraindications

Decreased level of consciousness without a protected airway

Craniofacial abnormalities

Concomitant head trauma

Other bodily injuries

If use increases the risk & severity of aspiration

If at risk of hemorrhage or GI perforation

Relative contraindication

If pt refuses to cooperate and resists

Complications may be more likely

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Complications:

summary of 2004 Position Paper

Aspiration pneumonia

Reported even in lower risk settings : when pts are awake, have been intubated or have ingested a nonhydrocarbon substance

Laryngospasm

Arrhythmia

Esophageal or stomach perforation

Fluid & electrolyte imbalance

Small conjunctival hemorrhages

Complications:

new studies

Gokel et al. (2010): documented electrolyte abnormalities associated with gastric lavage by prospectively monitoring serum Ca, ionized Ca, Mg, and Na at baseline, 15min, 6h, 12h after lavage in 30 patients presenting within 2h of amitriptyline poisoning

Decreases in serum Ca, ionized Ca, Mg but no clinical signs. Limit: pts were also receiving IVF

Griffiths et al. (2009): described a case of esophageal perforation as a complication of lavage in a pt who had taken 30 paracetamol-codeine & 20 asa.

No documentation other than “difficult procedure”

Complications:

new studies

Eddleston et al. (2007): observed gastric lavage in Sri Lanka

Noted many problems with supportive care resulting in high levels of complications (such as aspiration)

Several studies illustrating the risk in patients who have ingested hydrocarbons or pesticides

Jasyashree et al. (2006): identified predictors of poor outcome in 48 children with aliphatic hydrocarbon ingestion in India.

Those who had lavage had higher frequencies of hypoxemia, leukocytosis, need for mechanical ventilation

Wang et al. (2010): retrospectively identified predictors of pneumonia after cholinesterase poisoning in Taiwan. Lavage at a peripheral hospital where details of the procedure were not available vs at the study hospital with NGT lavage and activated charcoal given in lateral decubitus position.

Peripheral hospital 6.23 times more likely to develop pneumonia. Charcoal contamination of sputum was one of the main predictive factors for developing pneumonia

Indications- place in therapy:

summary of 2004 Position Paper

The evidence showing that gastric lavage provides therapeutic benefit to poisoned patients is weak

Experimental studies in animals and in humans show that lavage reduces bioavailability of markers in simulated overdose

Results are highly variable & diminish with elapsed time since ingestion

Clinical studies have failed to show that lavage improves the severity of illness, recovery time or the ultimate medical outcomes

Even when treatment is within 60 minutes

May be associated with a number of life-threatening complications: aspiration pneumonitis, aspiration pneumonia, esophageal or gastric perforation, fluid & electrolyte imbalances, arrhythmia

Should not be performed routinely if at all

In the rare situation that it might seem appropriate: clinicians should consider treatment with activated charcoal or observation & supportive care instead

No examples of when “gastric lavage might seem appropriate” were included

Indications- place in therapy: n

ew studies

Since 2004, there has been continued growth of medical literature showing that gastric lavage can cause harm to patients & very little demonstrating benefit

Nearly all studies showing benefit are written in

Chinese and are in the Chinese literature & were for organophosphorus pesticide poisoning

At present, evidence supporting situations were gastric lavage would be beneficial (ie: lethal ingestion, recent exposure, substance not bound to activated charcoal) is either based on theoretical grounds or case reports

Evidence to exclude gastric lavage in these scenarios is also lacking

Indications- place in therapy: n

ew studies

At least one indicator that clinicians might not be adequately equipped or skilled at performing gastric lavage

2010 UK study of hospital EDs found that 95% of respondents rarely or never performed gastric lavage; 50% said they did not have equipment; 38% said they did not have adequately skilled personnel available

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Indications- place in therapy: n

ew studies

Until methodologically sound clinical studies are published demonstrating or excluding that lavage hastens clinical recovery rates or improves patient outcomes, gastric lavage should not be performed routinely, if at all, for the treatment of poisoned patients

So…. All of that to say that the recommendations are the same as in 2004

Treatment of poisoned patients

Prehospital Triage to Primary

Stroke Centers and Rate of Stroke

Thrombolysis

JAMA 2013

IV tPA is the only evidence based treatment for ischemic stroke but it’s use remains low, 1-5%

Strategy to increase usage

Methods

The whole city is served by one EMS provider

Chicago Fire Department

Chicago Area Stroke Taskforce, 2007

Healthcare professionals, Chicago Fire, hospital administrators, government agencies, not for profits

Met quarterly

Passed a state law recommending preferential transportation of stroke patients to the nearest

Primary Stroke Center

Methods

Developed pre-hospital triage

Symptom onset < 6 hours, Cincinnati Stroke Score

All sorts of education ensued

Primary outcome was the rate of stoke thrombolysis

Secondarily, changes in use of EMS, EMS prenotification, onset-to-arrival time, onset-totreatment time, door-to-needle time, complications, in-hospital mortality

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Results

Increased arrival within 60 minutes

From 7.5% to 13.7% (p=0.001)

Increased administration of tPA

From 3.8% to 10.1% (p=<0.001)

Onset-to-treatment time decreased

From 171.7 minutes to 145.7 minutes (p=0.03)

Door-to-needle time did not change

Among those receiving tPA, symptomatic intracranial hemorrhage occurred in similar proportions

Discussion

The effect was associated with a near 30-minute reduction in onset-to-treatment time

They found these results have been sustained

Certainly there are opportunities for improvement with respect to education, process and reporting

26

The Current Understanding of

Stevens-Johnson Syndrome and Toxic Epidermal

Necrolysis

Maja Mochenhaupt, MD, PhD www.medscape.org/viewarticle/751622 10/21/11

SJS, SJS/TEN-overlap and TEN with macula are considered a single disease of different severity

EMM is different in terms of clinical pattern and in etiology

Introduction

Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are diseases within the spectrum of severe cutaneous adverse reactions

(SCAR) affecting skin and mucous membranes

Erythema multiforme with mucosal involvement, erythema multiforme majus (EEM) or bullous erythema multiforme is also part of the spectrum

A genetic predisposition for patients has long been suspected

Consensus definition: Bastuji-Garin et al. 1993 classification is based on the type of single lesions and on the extent of blisters or erosions related to

BSA

Clinical Pattern: SJS/TEN

Fever & malaise are often the first symptoms and may persist or increase once the muco-cutaneous lesions appear

Cutaneous erythema with blister formation of various extent

Hemorrhagic erosions of mucous membranes (such as stomatitis, balanitis, colpitis, severe conjunctivitis and blepharitis)

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Lesions: Consensus Definition

Typical targets

Regular round shape and a well-defined border with at least 3 different concentric zones

A purpuric central disk with or without a blister

A raised edematous intermediate ring

An erythematous outer ring

Atypical raised targets

Only 2 zones and a poorly defined border

Atypical flat targets

Vesiculous or bullous lesions in the center

May be confluent

Lesions

EMM

Typical or atypical raised targets are characteristic

SJS

Appear mainly on the limbs, but sometimes also the face and trunk, especially in children

Skin detachment is limited: often 1-2% of BSA

Widespread, often confluent purpuric macules (spots) or atypical flat targets

Predominantly on the trunk

Skin detachment: higher but <10% of BSA

TEN

Widespread macules and atypical targets usually preceded epidermal sloughing

Diagnosis requires skin detachment >30% of BSA

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Skin Detachment Positive Nikolsky sign

Direct Nikolsky sign

When the epidermis can be pushed slightly aside by pressure of fingers

Indirect Nikolsky sign

When an existing blister can be “pushed away” by pressure of fingers

1/19/2015

Hermorrhagic erosions

Hemorrhagic erosions of at least one site of mucous membranes are present in EMM, SJS, and

SJS/TEN overlap, but may be absent in some cases of TEN

Histopathology

Findings can distinguish SJS/TEN from other diseases, but do not allow the clear differentiation between SJS/TEN and EMM

Both show similar findings

What time the biopsy is taken in relation to the onset of the disease and from which part of the lesion is important

Differential Diagnosis

May vary with the clinical presentation and the extent of the skin detachment

Early stages: maculopapular eruptions induced by drugs or viruses

Later stages

MUST exclude Staph Scalded Skin

Syndrome

GBFDE (generalized bullous fixed drug eruption)

Autoimmune blistering diseases

Pemphigus vulgaris, bullous pemphigoid, bullous phototoxic reactions

 Erythroderma, exfoliative dermatitis, acute generalized exanthemic pustulosis

Incidence & Demographics

Incidence: 1-2 cases per million per year

Distribution in gender

SJS and TEN: almost equal

SJS/TEN overlap: 65% female

EMM: 70% males

Mortality

SJS: ~10%

SJS/TEN overlap: ~30%

TEN: ~50%

SJS, SJS/TEN, TEN

 overall mortality ~25%

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Etiology

Rarely occurs without any drug use

For most drugs, median latency time between beginning of drug use and onset of SJS/TEN was

< 4 weeks

In general no significant risk after 8 weeks

Viral infections and mycoplasma pneumonia were also reported as potential causes

SCAR study and

EuroSCAR study

NSAIDs: oxicam type are considered high risk to induce SJS/TEN

NSAIDs: acetic acid and propionic acid type are not

ALDEN

Numerical score values lead to causality assessment for each individual drug

Very unlikely

Unlikely

Possible

Probable

Very probable

Drugs could be identified as causes in no more than 75% of cases in these studies

25% of the cases, no drug could be determined

Antiepileptic drugs

• more than 90% of SJS/TEN cases occurred in the first 63 days of drug use

• Risk estimates vary between 1 and 10 per

10,000 for new users

• Valproic acid has much lower risk estimates

For antibiotics, anti-infective sulfonamides

(especially

TMP/SMX) have the highest risk

Pathophysiology & Genetics

Drugs are the etiological factor but it is still unknown how a certain drug induces epidermal necrosis

CD8 + Tcells have been identified to play a role in the process mediated by cytokines

The cytologic protein granulysin was identified in high concentrations in blister fluid

May be a marker of severity

A genetic predisposition for SJS/TEN has long been discussed

A 2004 Taiwan study demonstrated that 100% of Han-Chinese patients with SJS/TEN due to carbamazepine use were positive for the HLA-B*1502 allele

1/19/2015

Therapeutic Considerations

Based on nonspecific and symptomatic means

Topical Treatment

Leave blisters in place or only puncture

Erosions: chlorhexidine, octenisept or polyhexanide solutions and impregnated mesh gauze

Avoid silver sulfadiazine

Affected mucosal surfaces

Specialized care is critical

Oral erosions: disinfectant mouth wash and mild ointment

(dexpanthenol) for lips

Eye-involvement

Regular ophthalmologic consultation is crucial: even if eye involvement is not present initially!

Specialized lid care is needed daily and regular anti-inflammatory gtts

Supportive Care

Withdraw any drugs suspected of causing SJS/TEN

Room temperature should be increased (30-32˚C)

Bed on alternating pressure mattresses

Patients with skin detachment >30% have increased risk for different systemic complications

Highly specialized derm units, burn units or ICU with daily derm consultation are best options

Fluid replacement:

Only need 2/3 to 3/4 of the fluids of burn patients

 electrolyte (0.7ml/kg/%BSA) and albumin solution (5% human albumin,

1ml/kg/%BSA)

Food: po or tube feeds

Monitor for infections, if suspected, start emperical coverage

Sedation and analgesia as indicated

29

? Other Treatments

All either controversial and limited data

Glucocorticoids

 A controlled therapeutic trial should be undertaken

Intravenous immunoglobulins (IVIg)

Not the best treatment and generally cannot be recommended

Plasmapharesis

Hyperbaric oxygen

Cyclosporin

Acute Complications

Transdermal fluid loss → hypovolemia, changes in electrolyte levels and catabolic metabolism

Most dangerous: occurrence of infections

Septicemia is the most frequent cause of death in patients with SJS/TEN

One of the most severe complications is involvement of tracheal and bronchial epithelium

May develop in 20% of TEN patients

Hypoxemia, hypocapneia and metabolic alkalosis lead to mechanical ventilation, increases risk of death

Prognosis

 SCORTEN: Severity of Illness Score for Toxic

Epidermal Necrosis

Can evaluate prognosis of individual patients

Does not predict sequelae

Long-lasting Sequelae

Cutaneous

As long as the upper dermis is not affected by trauma or infection, the skin regenerates without atrophic or hypertrophic scars

Frequently have hyper- or hypopigmentation

 Pruritis, hyperhidrosis, xeroderma

Nail deformities

Mucosal

Depapillation of the tongue

Synechia

Impairment of taste

Women: vaginal adhesions, mucosal dryness, pruritis, bleeding of the genital mucosa

Eyes

Most severe sequelae

Chronic inflammation, entropion, fibrosis, trichiasis, symblepharon

 Visual loss, blindness

Summary

SJS/TEN and EMM are different conditions that are distinguished in clinical and etiological terms

SJS and TEN are the same disease, different severities

TEN diagnosis requires skin detachment >30% of BSA

SJS/TEN is mainly caused by drugs (up to 75% of cases), but also infections and other unknowns

High risk confirmed for: allopurinol, anti-infective sulfonamides, carbamazepine, phenytoin, phenobarbital and oxicam-

NSAIDs

Lamotrigine and nevirapine had highest risk of recently marketed drugs

Summary

Pathogenesis has not been completely solved

Certain genetic predispositions: HLA alleles identified

The cytologic protein granulysin may be a marker of severity

Supportive care is crucial but mortality is still high

Septicemia is the most frequent cause of death in patients with SJS/TEN

Survivors may suffer long term sequelae, including severe eye problems

1/19/2015

30

Be Prepared – Boston

Marathon and Mass-

Casualty Events

NEJM 2013

3 killed, 264 injured, 20 were critical

All victims transported from the scene within 45 minutes

Each of Boston’s major trauma centers received a relatively equal number of patients

No one who was transported to a hospital died

Boston Marathon

The success of the rescue efforts is attributed to the high level of preparedness and preparation on the part of the city of Boston’s medical community

Routinely, there are a number of medical tents set up at this event and they describe caring for upwards of 1000 medical situation in 6 hours

They routinely treat the marathon as a ‘planned mass-casualty event’ for training purposes

1/19/2015

Boston Marathon

They transformed one of their medical tents to a triage center where they were able to offer rapid treatment and transport

They used the tourniquet based on evidence from

Iraq and Afghanistan that it it dramatically reduces combat deaths from limb exsanguination

All ambulances were dispatched from a central location, private ambulances were called on to help

Boston Marathon

The first patients went out 18 minutes after the blast

Receiving hospitals initiated mass casualty protocols to free up their EDs and Ors

ED patients were transferred to the floors for a continuation of their work up by the inpatient team

The authors stress just how unfortunate it is that US health departments and EMS are facing federal budget cuts as this disaster would likely not have gone as smoothly without the high level of preparedness on Boston’s part

Immediate and Delayed

Traumatic Intracranial

Hemorrhage in Patients With Head

Trauma and Preinjury Warfarin or

Clopidogrel Use

Nishijima et al. Ann of Emerg Med.

2012;59:460-468.

June 2012

Background

The use of anticoagulants and antiplatelet agents, specifically warfarin and clopidogrel is steadily increasing

Previous studies suggest that patients receiving either of these medications are at increased risk for traumatic intracranial hemorrhage (tICH) but the risk in a large, generalizable cohort is unknown

Current guidelines recommend that patients with head trauma and preinjury warfarin undergo routine cranial CT imaging

Have not addressed preinjury clopidogrel

31

Importance

Majority of patients with tICH are identified on initial CT

Limited data suggests that patient receiving warfarin are at increased risk for delayed tICH

Not uncommon practice to reverse warfarin anticoagulation even with normal CT

Generated guidelines for routine CT and hospital admission

Evidence for clopidogrel is even more limited

Current guidelines do not explicitly recommend routine

CT for these patients after blunt head trauma

Risk for delayed tICH is unknown

Materials & Methods

Prospective, observational, multicenter study at

2 trauma centers and 4 community hospitals in

Northern California

Adult ≥18 ED patients with blunt head trauma

(regardless of LOC or amnesia) and preinjury warfarin or clopidogrel use within the previous 7 days

Excluded

 transferred patients with known tICH

Concomitant warfarin and clopidogrel use

1/19/2015

Data Collection & Processing

Treating ED physician recorded patient history & medication use, injury mechanism and clinical exam

GCS

Evidence of trauma above the clavicles

 At each site, ~10% of patients had a separate, independent faculty physician assessment to evaluate reliability of preselected clinical variables

Imaging studies were ordered at the discretion of the treating physician

Outcome Measures

EMRs were reviewed to assess INRs, CT results, ED disposition and hospital course

Patients admitted for at least 14 days were evaluated for the presence of delayed tICH through EMR review

Patients discharged from the ED or hospital <14 days had a phone survey

Repeated cranial imaging was at the discretion of the patients’ treating physicians

If unable to be contacted, the Social Security

Death Index was reviewed

Outcome Measures

Immediate tICH presence of any ICH or contusion as interpreted by the faculty radiologist on initial cranial CT scan

Delayed tICH tICH on cranial CT scan occurring within 14 days after and initial normal CT scan and in the absence of repeated head trauma

Neurosurgical intervention use of intracranial pressure monitor or brain tissue oxygen probe, placement of a burr hole, craniotomy/craniectomy, intraventricular catheter or subdural drain, or the use of mannitol or hypertonic saline solution

Results

Between April

2009 & January

2011

2 Trauma centers:

364 patients

4 Community hospitals: 700 patients

4/687 (0.6%) of warfarin cohort had delayed tICH

1000 had initial

ED CT

Prevalence of immediate tICH was higher for clopidogrel patients than warfarin

No delayed tICH in clopidogrel cohort

32

Results

In patients with immediate tICH,

10.8% of warfarin pts &

18.2% of clopidogrel pts had

• No LOC

• Normal mental state

• No evidence of trauma above the clavicles

Majority (87.6%) had

GCS of 15

Hospitalization rates were similar

Most common mechanisms of injury

1. Ground level fall

(83.3%)

2. Direct blow (5.6%)

3. MVC (4.8%)

Headache, concomitant aspirin use, and evidence of trauma to the neck and scalp laceration were more common in the clopidogrel group

Results: immediate tICH

tICH Higher in clopidogrel cohort

Mortality and neurosurgical intervention rates after tICH were not different

1/19/2015

Results: delayed tICH

All warfarin

2 were deemed nonoperable and died

Limitations

Observational study

CT scans were not obtained for all patients

Potentially had an undiagnosed tICH, although none identified on follow-up

Some patients with an negative initial CT may have eventually developed an undiagnosed delayed tICH

Did a subgroup analysis on the aspirin + clopidogrel patients

The absence of aspirin from the clopidogrel group did not significantly decrease the incidence for immediate traumatic hemorrhage in the clopidogrel group

Did not collect data on patients with isolated preinjury aspirin use or without preinjury antiplatelet or anticoagulation use

Patients on warfarin may be more acutely aware of bleeding risks, therefore may be more apt to seek ED care

Discussion

The prevalence of immediate traumatic intracranial hemorrhage in patients with clopidogrel was significantly higher compared with those receiving warfarin

The development of delayed traumatic ICH after a negative initial cranial CT scan is rare for warfarin and clopidogrel patients

Does not warrant routine hospitalization for observation or immediate anticoagulation reversal

? Change to Current

Guidelines

Current results indicate that head injured patients on warfarin and clopidogrel should be approached the same way

 Liberal cranial imaging

Because delayed diagnosis of tICH increases morbidity and mortality, early diagnosis of tICH is important to initiate treatment, including coagulopathy reversal or neurosurgical intervention

33

? Change to Current

Guidelines

Current NICE head injury guidelines recommend urgent

(<1h) CT in patients with head injury and preinjury warfarin use provided they sustain LOC or amnesia

Prevalence of immediate tICH in well-appearing patients is concerning

More than 60% of patients with immediate tICH in both warfarin and clopidogrel cohorts had a normal mental state

(GCS of 15)

A significant portion of patients had no LOC, a normal mental status, and no physical evidence of trauma above the clavicles

Recommend routine urgent CT imaging even in wellappearing patients without LOC or amnesia

? Change to Current

Guidelines

Concern for delayed tICH from case reports and case series led to guidelines recommending routine admission for all head-injured warfarin patients despite normal CT

Results show delayed tICH is infrequent (<1%) in both populations

Recommend if no other indications for admission, discharge home with explicit discharge instructions and close follow-up

1/19/2015

Reversal of warfarin?

 A 2005 survey of clinical practices of North

American trauma surgeons

74% of respondents reversed patients receiving warfarin despite normal cranial CT

66% used FFP

Results show delayed tICH is infrequent (<1%) in both populations

Recommend that these patients do not need to have their therapeutic anticoagulation aggressively reversed

If supratherapeutic INTs, use current guidelines

Summary

Immediate tICH: clopidogrel > warfarin

Routine cranial CT imaging is indicated in preinjury clopidogrel or warfarin patients with blunt head injury regardless of the clinical findings

Incidence of delayed tICH is very low

In patients with initial normal CT, do not reverse anticoagulation and discharge home with close follow-up

Thank you!

COLA 2014 for testing purposes

Shoot us an email with any questions or if you’d like a line on the articles

 jsteve10@hfhs.org

 hcronov1@hfhs.org

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35

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