COLA 11
(2014-2016)
HEATHER CRONOVICH, DO
JENNIFER STEVENSON, DO
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
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
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
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
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
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
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
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
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…
Blunt trauma results in the majority of bladder injuries
High association with pelvic injuries
Full vs. empty bladder
2
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
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
Require immediate surgical exploration
You don’t even want to know what they do here…
Can lead to testicular rupture or dislocation
Ultrasonography is recommended
Exploration is recommended in the event of equivocal ultrasound findings
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
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
Murthi et al.
Expert Review of Hematology. 2011;4(5):527-537
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
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
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
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
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 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
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
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
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
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%
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
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
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
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)
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?
Single- donor freeze dried plasma
Plasma-derived coagulation factor concentrates
TXA (tranexamic acid)
Fibrin bandages
Advances in patient monitoring
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
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
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
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
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
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
Time from randomization to the next medically confirmed episode of cellulitis
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
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
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
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
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
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
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
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
Litovitz et al.
Pediatrics 2010;125;1168; originally published online May 24, 2010; DOI:10.1542/peds.2009-3037
2010
9
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
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
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
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
(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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
(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
www.poison.org/battery/guidelines.asp
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
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)
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
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
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
Recurrent abscesses, sinus tract formation and scarring
Often treated with oral antibiotics with antiinflammatory properties
Androgens have been used based on antidotal evidence
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
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
Jeffrey I Cohen, M.D.
The New England Journal of
Medicine
N ENGL J MED 369;3
July 18, 2013
15
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?
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
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
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
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
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
1/19/2015
16
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
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
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
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
1/19/2015
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
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
17
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
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
Other treatments may be added:
• Mydriatric gtts
• Topical glucocorticoids
• Medications to reduce intraocular pressure
• Intravitreal antiviral therapy
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
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%
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
1/19/2015
18
Less contagious than varicella, but can still transmit VZV to susceptible persons
Use contact precautions and cover lesions if possible
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
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
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
Neurosurgery 2013
112 evidence based recommendations comparing the most current research with that from a decade ago
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
1/19/2015
19
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
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
1/19/2015
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
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
Traction is not recommended in the management of patients with AOD, and is associated with a
10% risk of neurological deterioration – Level I
The routine use of CT and MR imaging of trauma victims with ankylosing spondylitis is recommended, even after minor trauma - Level III
20
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
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 (?!)
1/19/2015
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
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
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
21
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
Benson et al.
Clinical Toxicology (2013), 51 , 140-146
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
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
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
new studies
No new studies since 2004
1/19/2015
22
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)
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)
No new studies
new studies
No new studies
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
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
1/19/2015
23
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
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
1/19/2015
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
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
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
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
24
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
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”
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
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
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
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
1/19/2015
25
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
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
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
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
1/19/2015
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
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
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
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
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)
1/19/2015
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
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
27
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
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
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
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: 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%
28
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
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
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
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
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
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
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
SCORTEN: Severity of Illness Score for Toxic
Epidermal Necrosis
Can evaluate prognosis of individual patients
Does not predict 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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
1/19/2015
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
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
Liberal cranial imaging
33
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
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
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
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
The Current Understanding of Stevens-Johnson
Syndrome and Toxic Epidermal
Necrolysis www.medscape.org/viewarticle/751622
10/21/11
Transfusion Medicine for Trauma Patients: An
Update www.medscape.org/viewarticle/749747
9/23/11
Herpes Zoster NEJM 2013; 369: 255-263 7/18/13
Hidradenitis Suppurativa NEJM 2012; 366: 158-164
1/12/12
Immediate and Delayed Traumatic Intracranial
Hemorrhage in Patients with Head Trauma and
Pre-injury Warfarin or Clopidogrel Use Ann Em
Med 59: 6: 460-468 June 2012
34
Prehospital Triage to Primary Stroke Centers and Rate of
Stroke
Thrombolysis http://archneur.jamanetwork.com/article.asp
x?articleid=1704352 JAMA Neurol. 2013; 70(9): 1126-1132
Position paper update: gastric lavage for gastrointestinal decontamination Clinical Toxicology (2013), 51 140-146
Introduction to the Guidelines for the Management of
Acute Cervical Spine and Spinal Cord
Injuries.
journals.lww.com/neurosurgery/toc/2013/03002Ma rch 2013
Be Prepared—The Boston Marathon and Mass Casualty
Events NEJM 2013; 368: 1958-1960
Penicillin to Prevent Recurrent Leg Cellulitis NEJM 2013 368
(18): 1695-1703
Urologic Trauma Guidelines: a 21st Century
Update http://www.medscape.org/viewarticle/72
7952 09/10
Emerging Battery-Ingestion Hazard: Clinical
Implications http://pediatrics.aappublications.org/ content/125/6/1168.long 05/10
1/19/2015
35