Transcript SHOCK - rEMERGs

SHOCK
Core Rounds August 7, 2003
Dr. Rob Hall PGY4
Dr. Gil Curry MD, FRCPC
JOHN-WEST
Shock Talk:
outline
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A few cases
Approach to and ddx of shock
Detailed review of major causes
Focus on septic, hypovolemic, cardiogenic
shock for literature review
• Controversies in management of sepsis,
hypovolemic shock, cardiogenic shock
“ Shock
is the transition
between illness and
death”
Definitions of Shock
• Clinical manifestations of the inability of
the circulatory system to adequately supply
tissues with nutrients and remove toxic
waste
• Inadequate blood flow secondary to
decreased cardiac output or mal-distributed
output that results in irreversible tissue
damage
Rosen’s Empiric Cirteria for the
Diagnosis of Shock:
4 out of 6 criteria
• Ill appearance or
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decreased LOC
HR > 100
RR > 22 or PC02 < 32
Base deficit < -5 or
lactate > 4
Urine output < 0.5
ml/kg/hr
Hypotension > 20 minute
duration
• NOTES
• Can be in shock
without being
hypotensive
• Base deficit = amount
of base required to
neutralize the pH
(normal is > -2)
Classification of Shock:
find your own way to classify shock and
remember the ddx
• Pre - heart
• hypovolemia, venous
pooling
• Heart
• contractility, arrythmias,
mech obstruction
• Post - heart
• loss of vascular tone,
inability to deliver to
tissues, inability of tissues
to utilize
• Quantitative
• hypovolemic,
hemorrhagic,
obstructive, myocardial
dysfunction
• Qualitative
• sepsis, anaphylaxis,
neurogenic,
dyshemoglobinemia,
cellular poisons
Etiological Classification:
man this guy looks SSHHOCCKE…
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S
S
H
H
O
C
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• C • K • E -
septic
spinal (neurogenic)
hypovolemic
hemorrhagic
obstructive (PE, pthrx, hthrx, ct)
cardiogenic (rate, contractility,
obstruction, valve)
cellular toxins (CN, CO, HS, ASA, Fe)
anaphylaCTic
endocrine/adrenal crisis
Pathophysiology
• Common final pathway = cellular injury
• FIVE unifying features of shock
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intracellular calcium overload
intracellular hydrogen ion
cellular and interstitial edema
catabolic metabolism
inflammation
Undifferentiated Shock:
Thorough history, complete physical, shot gun
investigations………ya, but what are some tips?
• History
• Paramedics, caregivers, witnesses, family, and old chart
are keys to give you historical clues
• Get someone on the phone EARLY (ie: in resusc bay)
who can tell you what was going on
• Physical
• Don’t forget the chemstrip, rectal, AAA exam
• Investigations
• STAT echo can be very useful
• Emerg ultrasound will soon be available
Shock Trivia
• Patient in shock but is bradycardic: why?
• Elderly, medications, neurogenic shock, intraabdominal
pathology (vagal tone)
• Shock index
• HR/SBP > 0.9 suggest shock
• Lactate clearance index
• Patient is under – resuscitated if lactate has not
decreased by 50% since last measurement
• Gastric/Rectal Tonography
• Balloon probe measure mucosal pH as an indicator of
gut perfusion
Septic Shock
Definitions:
Consensus conference on definitions for sepsis: Critical Care
Medicine 2000. Volume 28 (1): 232 - 235
• SIRS (Systemic Inflammatory Response Syndrome)
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temp > 38 or < 36
HR > 90
RR > 20 or PaC02 < 32
wbc > 12, < 4, or > 10% bands
• Sepsis = SIRS + documented infection
• Severe Sepsis = Sepsis + MODS (Mulitorgan dysfuntion)
• Septic Shock = Sepsis + Hypotension refractory to volume
resuscitation (requiring vasopressors)
Management of Septic Shock
• Intubate/ventilate
• Control airway
• Decrease work of breathing
• Fluids
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Boluses of NS or RL
Adults: bolus 1-2 L and repeat
Peds: bolus 20 ml/kg and repeat
Pressors after 2-3 boluses but keep fluids running
Require a lot of fluid
• Absolute hypovolemia: increase incensibles, poor intake
• Relative hypovolemia: vasodilation and decreased SVR
Vasopressors:
Most common choices
• Dopamine:
• 1-5 ug/kg/min ~
dopaminergic
• 5-10 ug/kg/min ~ beta
activity
• >10 ug/kg/min ~ alpha
activity
• Preferred agent for many
• Effects well established
• Physicians comfortable
with use
• Levophed:
• 0.01 – 3 ug/kg/min
• Potent alpha agonist
• Some beta
propertiesConcern with
levophed worsening end
organ hypoperfusion
• Older studies: levophed
used as last resort and thus
poor outcomes
• Hesselvik JF, et al., Crit
Care Med 1989
Norepinephrine
• Norepinephrine improves renal blood flow
and tissue oxygenation in patients with
septic shock:
• Desjars et al., Crit Care Med 1989
• Rendl-Wenzel et al., Intensive Care Med
1993.
• Meadows et al., Crit Care Med 1988
• Martin C., et al., Crit Care Medicine 2000
Dopamine versus norepinephrine
• Martin et al., Chest 1993 and Marik et al., JAMA
1994
• Many small studies (n=20) like these two that showed a
benenfit in physiological markers with norepinephrine
• Levophed has favourable effect on hemodynamics
and end organ perfusion as compared to
dopamine
• A mortality benefit for levophed over dopamine
has never been shown
Pressor summary
• Make sure the pump is full first
• Dopamine/Levophed first line agents
• Levophed may be the superior agent in
septic shock
• Titrate up doses fast (q 5-10 min to effect)
• Add second agent if needed
• Invasive monitoring required
Sepsis and Antibiotics
• Bochud et al., Intensive Care Medicine 2001: reviewed 4
retrospective studies of septic patients and abx choice
• N=1190
• Appropriate Abx mort rate~28%
• Inappropriate Abx mot rate~49%
• P<0.001
• Early ED antibiotics have also shown to decrease
mortality in many disease subgroups (pneumonia,
meningitis, urosepsis)
EARLY and APPROPRIATE
initiation of antibiotic coverage
are CRUCIAL emergency
department interventions in the
patient with septic shock
Empirical antibiotic choices
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Target suspected source of infection
Refer to SANDFORD’s recommendations
Use maximum doses of antibiotics
Broad spectrum = grm +ves, grm –ves, anaerobes
Amp + Gent + Flagyl
Piperacillin/Tazobactam being used more often
Imipenum as monotherapy (big gun)
Neutropenic: cover pseudomonas (ceftazidime,
cipro, tobramycin)
Newer approaches to
septic shock:
• Vasoactive mediators
• vasopressin, nitric oxide
• Coagulation Cascade
• protein C, protein S, antithrombin III
• Inflammatory mediators
• anti TNF antibodies, anti LPS, TFPI,
interleukins, IVIG
Question: how to get an
intensivist talking at a wine and
cheese party?
Answer: just say……
(i) There is NO evidence for steroid
use in septic shock
(ii) Recombinant activated Protein C
is killing patients
Steroids in septic shock
Rationale:
• Anti-inflammatory
• Relative adrenal insufficiency in many of
cases of refractory shock
• Upregulates catecholamine receptors
• Hopefully immunosuppression and bleed
risk did not counter benefits
Steroids and Sepsis
• Early mega-dose
steroid trials
• “supraphysiologic”
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doses
Solumedrol 30/mg/kg
x 3-4 doses
Trend towards
increased mortality
Increase incidence of
GI bleeding
Increased incidence of
secondary infections
• 1990’s trial’s with
lower dose steroids
• “physiologic doses”
• aimed to replace
steroids for a “Relative
adrenal insufficiency”
• Researchers hoped get
catecholamine
sensitivity and antiinflammatory effects
still
Steroids and Sepsis:
Bollaert et al.,Critical Care Medicine 1998
• Double-blind, placebo controlled, small study
• Solu-cortef 100mg IV q 8hrs x 5days vs. placebo
• Outcome
Steroid group
Placebo
• Shock reversal @7d:
• Mortality
68%
32%
21% p=.007
63% p=.09
• No increase adverse outcomes
• Showed more shock reversal at 7 days with low
dose steroids
Steroids and Sepsis:
Briegel et al., Crit Care Med 1999.
• Another small RCT (n=40)
• Randomized to solu-cortef 100mg IV then low
dose infusion vs placebo
• Outcome
Steroid group Placebo
• Time to shock reversal 2 days
7 days (p=.005)
• No increase adverse outcomes, no diff in mortality
• Showed earlier shock reversal with low dose
steroids
Steroids and Sepsis:
Annane. JAMA 2002.
• Largest prospective trial of low dose steroids
• RCT, blinded, N = 300
• Randomized to low dose hydrocortisone (50 mg iv
q6hr) + fluticasone vs placebo
• Did ACTH stim test on everyone
• Mortality decreased 10% in “non-responders”
• 63% -> 53% (p = 0.02)
• Criticisms of their definitions of non-responders
and how they did the stim test exist
Steroids and Sepsis:
Review article in Chest May 2003
• High dose steroids clearly shown to
increase mortality
• There is some evidence for benefit from low
dose steroids in sepsis
• Current debate over low dose steroids
unresolved and needs further study
Steroids and Sepsis:
Take home message
• There is no current indication for the ED
initiation of low dose steroids in sepsis
unless adrenal crisis is suspected
• You should be aware that ICU will likely do
an ACTH stim test and may give steroids
Activated Protein C and Sepsis
• Antithrombotic
• Profibrinolytic
• Antiinflammatory
Activated Protein C and Sepsis:
drotrecogion (Zigris)
• PROWESS TRIAL (Bernard. NEJM 2001)
• Multicentered RCT, N = 1690
• Mortality 30.8% in placebo, 24.7% in treatment
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group (p= 0.005)
ARR 6.1% for NNT 16
RRR of 19%
Serious bleeding 3.5% vs 2.0% (p=0.06)
Enrollement criteria changed ½ way through!
Activated Protein C and Sepsis
• The FDA is confused
• Study stopped early because of “remarkable effect”,
FDA approved the drug
• Further discussion and controversy: FDA limited its use
to only sicker patients (based on APACHE score) and
asked for further study
• Critical Care Medicine. 31(1). S85-96
• Recent review on rhAPC
• Highlights problems with PROWESS study and FDA
approval --------- calls for further study
Activated Protein C and Sepsis
• Take home messages:
• rhAPC is expensive (10,000 per course)
• rhAPC has been shown to decrease mortality
although the effect is modest (ARR 6%)
• There is NO role for ED initiation of rhAPC
• May be used in ICU
Case
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15 yo male
Attempted hanging
Cut down from tree
HR 75, BP 85/30
Why is he in shock?
Neurogenic Shock:
Definitions
• Spinal Shock
• initial loss of spinal cord function following
SCI including motor, sensory, and sympathetic
function
• Neurogenic Shock
• loss of sympathetic autonomic function due to
spinal cord injury
Neurogenic Shock:
Pathophysiology
• Hypotension
• Due to loss of sympathetic tone thus vasodilation and
decreased SVR
• Usually only occurs with lesions at or above T6
because lower lesions leave enough of the body with
intact sympathetics that the BP doesn’t drop
• Bradycardia (absolute or relative)
• Due to unopposed parasympathetic (VAGAL) tone to
the heart
• Usually only occurs with lesions at or above T4
because sympathetic innervation to heart is at T4
Neurogenic Shock:
Management
• Fluids
• Atropine 0.5 mg – 1.0 mg iv
• NOTE: may see bradycardia or bradyasystolic arrest
due to stimulation from laryngoscopy so have atropine
ready if intubating
• Vasopressors
• Epinephrine 1:10,000 (1ml prn to effect)
• Phenylephrine: 10 mg in 100ml NS (1ml is 100 ug)
• Ephedrine
Hemorrhagic Shock
Hemorrhagic Shock:
Classification
Class I
Class II
Class III
Class IV
Volume
<750ml
750 – 1500 1500-2000 > 2000
%
< 15%
15-30%
30-40%
> 40%
HR
< 100
100 - 120
120 – 140
> 140
PP
N or incrd
decreased
decreased
decreased
BP
normal
normal
decreased
decreased
LOC
anxious
anxious
confused
lethargic
Hemorrhagic Shock:
Definition
• Hemorrhage vs Hemorrhagic shock?
• Rosen’s definition of hemorrhagic shock =
Requires 4 out of 6 empiric criteria for shock
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Ill or decreased LOC
U/o < 0.5 ml/kg/hr
HR > 100
RR > 22 or PC02 < 32
BD < -5 or lactate > 4
Hypotension > 20 minutes
Hemorrhagic Shock:
Management
• V: vascular access, crystalloid bolus X 2,
blood transfusion prn, identify and treat
cause
• Controversies
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Which fluid?
When to fluid resuscitate?
How fast should fluid be given?
Optimal endpoints of resuscitation?
Blunt versus penetrating trauma
Hemorrhagic Shock
Which fluid to give?
Colloids
• Albumin, protoplasm protein fraction,
hydroxyethylstarch, pentastarch, gelatin,
dextran
• Advantages
• less fluid required, more volume in vascular
space, potential to draw fluid in from tissues
• Disadvantages
• expensive, allergic reactions, coagulopathies
Colloids
• Cochrane Database of Systematic Reviews.
BMJ 1998: 317:235-40.
• Objective: effect of albumin on mortality
• Study: 30 RCTs total 1419 patients
• Results: RR of death 1.46 hypovolemia, 2.40
burns, 1.69 hypoalbuminemia
• Pooled RR of death 1.68 (1.26,2.23)
• Conclusion: albumin increases mortality
Colloids
• Cochrane Database 2003. Colloids versus
crystalloids for fluid resuscitation.
• Albumin:
18RCTs
RR1.52 (1.08,2.13)
• HES:
7 RCTs
RR 1.16 (0.68,1.96)
• Gelatin:
4 RCTs
RR 0.50(.08,3.03)
• Dextran:
8 RCTs
RR 1.24 (.94,1.65)
• Conclusion: No evidence that colloids reduce
risk of death in trauma, burns, or surgery
Colloids:
Summary
• There is NO evidence that colloids decrease
mortality in the resuscitation of critically ill
patients.
Hypertonic Saline
• Advantages
• less volume, stays in vascular space, draws fluid
• Disadvantages
• hypernatremia, hyperosmolarity, seizures,
coagulopathy, anaphylactoid rxns with dextran
• Details
• Hypertonic saline (7.5% NaCl) +/- 6% dextran
• Most often given as a 250 cc bolus (~ 4ml/kg) over 510 min
Hypertonic Saline
• Animal evidence
• improved hemodynamics and mortality
• Human evidence: Wade et al 1997:
• HS and HSD in trauma patients
• Metanalysis of 8 RCTS of HSD and 6 HS
• HS (7.5% saline): no difference in mortality
• HSD (+6%dextran): decreased mortality in 7/8
trials overall 3.5%; trend only ---> Not stat sign
Hypertonic Saline
• Cochrane Database 2003. Alderson P. Colloids vs
crystalloids for fluid resuscitation.
• Part of this systemic review looked at Hypertonic
Saline + Dextran and effect on mortality
• Study: metanalysis of 8 RCTs
• Results: pooled RR of 0.88 (0.74, 1.05)
• Conclusion: there is a trend toward reduction in
mortality with HSD although not statistically
significant
Hypertonic Saline
• Cochrane Database: 2003. Bunn F.
Hypertonic vs Isotonic Crystalloid
• 17 RCTs with total N = 869 (small trials!)
• 12/17 reported on mortality rates
• Trauma: RR death 0.84 (.61 – 1.16)
• Trend that favors hypertonic saline
Hypertonic Saline:
Conclusions
• There is evidence of TRENDS toward lower
mortality in resuscitation with hypertonic
saline but statistical significance has not
been demonstrated in large studies
• More RCTs are needed………..
Hemorrhagic Shock
When to give fluids?
How much?
How fast?
Controlled Fluid Resuscitation:
Rationale
• Also called hypotensive resuscitation or
permissive hypotension
• Elevation of BP before hemorrhage control
may be harmful
• Reasons
• Hydraulic pressure
• Dislodgement of soft clots
• Dilution of clotting factors
Controlled Fluid Resuscitation:
Evidence
• Early anmimal studies of fluid replacement
were in CONTROLLED hemorrhage
models showed benefit for fluids
• Recent animal studies of fluid replacement
in UNCONTROLLED hemorrhage models
show increased mortality with early and
aggressive fluids (especially if BP is
elevated)
Controlled Fluid Resuscitation:
Evidence
• Review articles:
• Emerg Med Clinics: 123(4). Nov 2002
• Journal of Trauma supplement Vol 54(5S). May
2003.
Bickell et al and Controlled Fluid
Resuscitation - “here
piggy,piggy”
Bickell et al 1990
The Detrimental Effects of Intravenous Crystalloid after
Aortotomy in Swine. Surgery 110: 529-36.
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Objective: does rapid volume replacement inc mortality?
Study: 16 pigs, 8 controls (no fluid), 8 tx (RL 80 ml/kg )
Results
Mortality
Controls
0/8
RL tx grp
8/8
Then repeated the study with hypertonic saline + dextran
Bickell et al 1992. HSD vs RL after Aortotomy
HSD tx grp
5/8
Bickell et al. NEJM 1994.
Immediate versus Delayed Fluid Resuscitation for
Hypotensive Patients with Penetrating Torso Trauma
• Study: 598 patients SBP<90, odd/even day
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randomization, immediate fluids vs none until OR
Immediate fluids - mortality 110/303 (38%)
Delayed fluids
- mortality 86/289 (30%)
Statistically significant p = 0.04
Concln: delayed fluid resuscitation reduces
mortality in hypotensive patients with penetration
Comments: even/odd day randomization,
significant cross over between groups, note short
transport times
Controlled Fluid Resuscitation:
What about blunt trauma?
• Turner. Health Technol Assess 2000.
Prehospital fluid replacement in serious
truama.
• RCT, immediate resuscitation vs no prehospital
fluids in blunt trauma
• N = 1309
• No diff in mortality, complications
• Hard to draw conclusions -> MAJOR protocol
violations
Controlled Fluid Resuscitation:
What about blunt trauma?
• Sampalis. J Trauma 1997
• Retrospective evidence of increased mortality
with IV therapy (? Due to longer scene time)
• Dutton. Resuscitation 1996
• Retrospective evidence of increased mortality
of rapid iv infusion compared to historical
controls
Controlled Fluid Resuscitation:
What about blunt trauma?
• Dutton RP. J. Trauma 2002. Hypotensive
Resuscitation During Active Hemorrhage:
Impact on in Hospital Mortality
• RCT, N=40, target SBP >70 or > 100
• ½ penetrating and ½ blunt trauma
• No difference in survival
• Small study, heterogenous patients, low
mortality
Controlled Fluid Resuscitation
• Cochrane Database 2001. Kwan I. Timing and
volume of fluid administration for patients with
bleeding following trauma.
• 3 RCTs for early vs delayed fluids
• 3 RCTs for large vs small volume
• NO evidence for early or large volume fluid
replacement and trends toward increased mortality
• But only 6 studies thus not a valid systemic review
Controlled Fluid Resuscitation:
Take home messages
• Early, aggressive fluid resuscitation increases
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mortality in penetrating trauma.
Controlled fluid resuscitation probably better
(target SBP 70 – 90)
Delayed fluid resuscitation (until hemmorrhage
controlled) may be better
Further study needed especially in blunt trauma
Unknown if this applies to long transport times
Pour it in for arrested or near-arrested patients
Where will trauma resuscitation
be in 2010?
My prediction: small volume of
hypertonic saline + dextran for target
SBP 90 and to OR ASAP!
Cardiogenic Shock
Cardiogenic shock
• Definition
• decreased cardiac output and evidence of tissue hypoxia
in presence of adequate intravascular volume
• Criteria
• hypotension (SBP < 90) x 30 min, or 30mmHG below
baseline, cardiac index < 2.2 L/min/m2, PCWP > 15
mmHg
• Rosen’s: 4 out of 6 criteria for empiric shock
• Pathologically
• Will have lost 40% of myocardium
Cardiogenic Shock
Etiology of Cardiogenic
Shock
Rate
Contractility
Valve
Obstruction
Brady
Tachy
Ischemia
Myocarditis
-ve ionotrope
CM or CHD
Acute rupture
Critical AS
Critical HOCM
Mech valve
PE
Tamponade
Tumor
Cardiogenic Shock:
Approach
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Stabilize the ABCs
Identify etiology of cardiogenic shock
Small fluid bolus (250cc)
Don’t be shy on fluids if RV infarct
Ionotropic/vasopressor support
Manage infarct
Cardiogenic shock:
Pressor choices
• Dobutamine: beta adrenergic
• positive B1 ionotrope; may drop BP b/c of vasodilation
• SBP 70 - 100 without signs of hypoperfusion a/f fluids
• Dopamine: dopaminergic, beta , alpha adrenergic
• SBP 70 - 100 with signs of hypoperfusion after fluids
• Norepinephrine: alpha agonist
• SBP < 70 after fluids
• Others
• Amrinone, milrinone
MI + Cardiogenic shock:
How to manage the MI?
• Options
• Thrombolysis
• Get BP up with ionotropes then thrombolyse
• Stabilize with IABP then thrombolyse
• PTCA
• Emergency CABG
• What does the literature tell us?
MI + Cardiogenic shock:
How to manage the MI?
• Thrombolysis in cardiogenic shock
• GISSI (N=280)
• streptokinase
• medical mx
30day mortality
70.1%
69.6%
• NO trial has shown reduction mortality with
cardiogenic shock with thrombolysis
MI + Cardiogenic shock:
How to manage the MI?
• Intra-Aortic Balloon Pump
• Gusto I: early IABP + lysis showed trend
towards lowered 30d and one year mortality
• SHOCK trial: IABP + lysis mortality 17%
versus medical mx alone 32%
• Temporizing with IABP then lysis is an
option
Cardiogenic: the SHOCK trial
Hochman JS. NEJM 1999; vol 341 (9): 625-34.
• RCT of AMI + cardiogenic shock
• 152 early revascularization (PTCA or CABG)
or 150 initial medical mx only (lysis initially,
some had PTCA/CABG after 52hrs)
• End Point early revasc. Med Mx stats
• 30d mortality 46.7%
56%
p=.11
• 6m mortality 50.3%
63.1%
p=.027
Cardiogenic Shock:
the SHOCK trial
• Hochman JS. One year survival following
early revascularization for cardiogenic
shock. JAMA 2001.
• End Point early revasc. Med Mx stats
• 1yr survival 46.7%
33.6% p=.03
MI + Cardiogenic shock:
How to manage the MI?
• Conclusions …….
• Patients with AMI complicated by cardiogenic
shock, especially those < 75yo, should undergo
emergent revascularization (PTCA or CABG)
Anaphylactic Shock
• You’d better know this!
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Airway management
Epinephrine
Benadryl
Fluids
Steroids
Racemic epinephrine and ventolin nebs
Ranitidine
Glucagon
Etiology of Adrenal Crisis
Underlying
Adrenal
Insufficiency
(Addision’s and
Chronic Steriods)
Acute
Precipitant
Adrenal
Crisis
Acute adrenal crisis?
• Underlying Adrenal
insufficiency
• Addison’s disease
• Chronic steroids
• No underlying Adrenal
insufficiency
• Adrenal infarct or
hemorrhage
• Pituitary infarct or
hemorrhage
• Precipitants of Adrenal
crisis
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Surgery
Anesthesia
Procedures
Infection
MI/CVA/PE
Alcohol/drugs
Hypothermia
Key Features of Adrenal Crisis
• Nonspecific
• Nausea, vomiting,
abdominal pain
• Shock
• Distributive shock not
responsive to fluids or
pressors
• Laboratory (variable)
• Hyponatremia,
hyperkalemia, metabolic
acidosis
• Known Adrenal
insufficiency
• Features of
undiagnosed adrenal
insufficiency
• Weakness, fatigue,
weight loss, anorexia,
N/V, abdo pain, salt
craving,
hyperpigmentation
Features of Adrenal Insufficiency
PRIMARY
ADRENAL INSUFF
SECONDARY /
TERTIARY ADRENAL
INSUFFICIENCY
Hyperpigmentation
Hyponatremia
Hyperkalemia
Metabolic Acidosis
NO Hyperpigmentation
Mild hyponatremia
NO hyperkalemia
NO met acidosis
Adrenal Crisis
• Consider on the
differential diagnosis of
SHOCK NYD
Management of Adrenal Crisis
• Corticosteroid replacement
• Dexamethasone 4mg iv q6hr is the drug of choice
(doesn’t affect ACTH stim test)
• Hydrocortisone 100 mg iv is an option
• Mineralocorticoid not required in acute phase
• Other
• Correct lytes, fluid resuscitation (2-3L)
• Glucose for hypoglycemia
• Pressors
Conclusions
• Shock is the transition between illness and
death
• Shock has many different causes but the end
result is the same
• The diagnosis and management of shock is
essential knowledge in emergency medicine