SHOCK

1
SHOCK

• Core Rounds August 7, 2003
• Dr. Rob Hall PGY4
• Dr. Gil Curry MD, FRCPC

2
Shock Talkoutline

• 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

3
Shock is the transition between illness and
death
4
Collapse at triage

• 40 yo female, mentally challenged
• Collapses at triage No history available
• Looks shocky, altered LOC, HR 130, BP 70 palp,
  Sats 88, RR 30, C/S 7, Temp 38.2
• General exam no focal neuro abnormality, neck
  supple, pelvic normal, abdo soft but ? Diffuse
  tenderness, chest clear, ? Flow murmur, no signs
  of endocarditis
• Old chart 3 weeks post dc (day surgery) RA
• Pharmacy print out steroid Rx
• Wbc 20, pH 7.2, lactate 5, ECG sinus tach, CXR
  clear, urine dip clear

5
Case 1

• 23 yo female, CC collapsed with abdominal pain
  at wedding
• VS at triage BP 110/70, pulse 84, in mild
  distress
• 1 hour later physician assessment
• Anxious, clammy, BP 70/50, pulse 90
• ? Additional history
• ? Investigations
• ? Management

6
Case 2

• 88yo male CC chills, fever, malaise with triage
  vitals BP 130/94, HR 110 T38.6
• PMHx Afib, MI, CHF, HTN, COPD, dementia
• Multiple CV meds including warfarin
• W/u wbcs in urine, normal CXR, unchanged ECG,
  enlarged nontender prostate, stool OB ve, WBC 18
• 2hrs later BP drops to 85 systolic, pulse 120
• Ddx
• Management

7
Case 3

• You are called STAT to front door of ED to assist
  in extrication of patient from a car
• You find a young man who is pale, opens eyes to
  command, but has only thready rapid carotid
  pulse. Chest is clear.
• The driver says pt. Felt sick while eating a
  salad in a restaurant and asked to be driven to
  the hospital
• Ddx
• Mx

8
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

9
Rosens Empiric Cirteria for the Diagnosis of
Shock 4 out of 6 criteria

• Ill appearance or decreased LOC
• HR gt 100
• RR gt 22 or PC02 lt 32
• Base deficit lt -5 or lactate gt 4
• Urine output lt 0.5 ml/kg/hr
• Hypotension gt 20 minute duration

• NOTES
• Can be in shock without being hypotensive
• Base deficit amount of base required to
  neutralize the pH (normal is gt -2)

10
Classification of Shock find your own way to
classify shock and remember the ddx

• Quantitative
• hypovolemic, hemorrhagic, obstructive, myocardial
  dysfunction
• Qualitative
• sepsis, anaphylaxis, neurogenic,
  dyshemoglobinemia, cellular poisons

• 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

11
Etiological Classification man this guy looks
SSHHOCCKE

• S - septic
• S - spinal (neurogenic)
• H - hypovolemic
• H - hemorrhagic
• O - obstructive (PE, pthrx, hthrx, ct)
• C - cardiogenic (rate, contractility,
  
  
  
  obstruction, valve)
• C - cellular toxins (CN, CO, HS, ASA, Fe)
• K - anaphylaCTic
• E - endocrine/adrenal crisis

12
Pediatric Shock same ddx but few caveats

• S - septic
• S - spinal (neurogenic)
• H - hypovolemic gastro, abdo surgical
  emergency, DKA
• H - hemorrhagic
• O - obstructive (PE, pthrx, hthrx, ct)
• C - cardiogenic (rate- SVT, contractility,
  
  
  
  obstruction, valve, congential heart dz)
• C - cellular toxins (CN, CO, HS, ASA, Fe)
• K - anaphylaCTic
• E - endocrine adrenal crisis (CAH)
  /hypoglcemia/metabolic defects

13
Pathophysiology

• Common final pathway cellular injury
• FIVE unifying features of shock
• intracellular calcium overload
• intracellular hydrogen ion
• cellular and interstitial edema
• catabolic metabolism
• inflammation

14
Undifferentiated Shock Thorough history,
complete physical, shot gun investigationsya,
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
• Dont forget the chemstrip, rectal, AAA exam
• Investigations
• STAT echo can be very useful
• Emerg ultrasound will soon be available

15
Shock Trivia

• Patient in shock but is bradycardic why?
• Elderly, medications, neurogenic shock,
  intraabdominal pathology (vagal tone)
• Shock index
• HR/SBP gt 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

16
Septic Shock
17
DefinitionsConsensus conference on definitions
for sepsis Critical Care Medicine 2000. Volume
28 (1) 232 - 235

• SIRS (Systemic Inflammatory Response Syndrome)
• temp gt 38 or lt 36
• HR gt 90
• RR gt 20 or PaC02 lt 32
• wbc gt 12, lt 4, or gt 10 bands
• Sepsis SIRS documented infection
• Severe Sepsis Sepsis MODS (Mulitorgan
  dysfuntion)
• Septic Shock Sepsis Hypotension refractory to
  volume resuscitation (requiring vasopressors)

18
Management of Septic Shock

• Intubate/ventilate
• Control airway
• Decrease work of breathing
• Fluids
• 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

19
VasopressorsMost common choices

• Dopamine
• 1-5 ug/kg/min dopaminergic
• 5-10 ug/kg/min beta activity
• gt10 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 properties
• Concern 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

20
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

21
Dopamine versus norepinephrine

• Martin et al., Chest 1993 and Marik et al., JAMA
  1994
• Many small studies (n20) 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

22
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

23
Sepsis and Antibiotics

• Bochud et al., Intensive Care Medicine 2001
  reviewed 4 retrospective studies of septic
  patients and abx choice
• N1190
• Appropriate Abx mort rate28
• Inappropriate Abx mot rate49
• Plt0.001
• Early ED antibiotics have also shown to decrease
  mortality in many disease subgroups (pneumonia,
  meningitis, urosepsis)

24
EARLY and APPROPRIATE initiation of antibiotic
coverage are CRUCIAL emergency department
interventions in the patient with septic shock
25
Empirical antibiotic choices

• Target suspected source of infection
• Refer to SANDFORDs 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)

26
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

27
Question how to get an intensivist talking at a
wine and cheese party?

• Answer just say
• There is NO evidence for steroid use in septic
  shock
• Recombinant activated Protein C is killing
  patients

28
Steroids in septic shock

• Rationale
• Anti-inflammatory
• Relative adrenal insufficiency in many of cases
  of refractory shock
• Upregulates catecholamine receptors

29
Steroids and Sepsis

• Early mega-dose steroid trials
• supraphysiologic doses
• Solumedrol 30/mg/kg x 3-4 doses
• Trend towards increased mortality
• Increase incidence of GI bleeding
• Increased incidence of secondary infections

• 1990s trials with lower dose steroids
• physiologic doses
• aimed to replace steroids for a Relative adrenal
  insufficiency
• Researchers hoped get catecholamine sensitivity
  and anti-inflammatory effects still

30
Steroids and SepsisBollaert 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 _at_7d 68 21 p.007
• Mortality 32 63 p.09
• No increase adverse outcomes
• Showed more shock reversal at 7 days with low
  dose steroids

31
Steroids and Sepsis Briegel et al., Crit Care
Med 1999.

• Another small RCT (n40)
• 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

32
Steroids and SepsisAnnane. 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 -gt 53 (p 0.02)
• Criticisms of their definitions of non-responders
  and how they did the stim test exist

33
Steroids and SepsisReview 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

34
Steroids and SepsisTake 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

35
Activated Protein C and Sepsis

• Antithrombotic
• Profibrinolytic
• Anti-inflammatory

36
Activated Protein C and Sepsisdrotrecogion
(Zigris)

• PROWESS TRIAL (Bernard. NEJM 2001)
• Multicentered RCT, N 1690
• Mortality 30.8 in placebo, 24.7 in treatment
  group (p 0.005)
• ARR 6.1 for NNT 16
• RRR of 19
• Serious bleeding 3.5 vs 2.0 (p0.06)
• Enrollement criteria changed ½ way through!

37
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

38
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

39
Case

• 15 yo male
• Attempted hanging
• Cut down from tree
• HR 75, BP 85/30
• Why is he in shock?

40
Neurogenic ShockDefinitions

• 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

41
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 doesnt 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

42
Neurogenic ShockManagement

• 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 110,000 (1ml prn to effect)
• Phenylephrine 10 mg in 100ml NS (1ml is 100 ug)
• Ephedrine

43
Hemorrhagic Shock

• Do you think this guy might be in shock?

44
Hemorrhagic ShockClassification
45
Hemorrhagic ShockDefinition

• Hemorrhage vs Hemorrhagic shock?
• Rosens definition of hemorrhagic shock
  Requires 4 out of 6 empiric criteria for shock
• Ill or decreased LOC
• U/o lt 0.5 ml/kg/hr
• HR gt 100
• RR gt 22 or PC02 lt 32
• BD lt -5 or lactate gt 4
• Hypotension gt 20 minutes

46
Hemorrhagic Shock Management

• Vascular access, crystalloid bolus X 2, blood
  transfusion prn, identify and treat cause
• Controversies
• Which fluid?
• When to fluid resuscitate?
• How fast should fluid be given?
• Optimal endpoints of resuscitation?
• Blunt versus penetrating trauma

47
Hemorrhagic Shock

• Which fluid to give?

48
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

49
Colloids

• Cochrane Database of Systematic Reviews. BMJ
  1998 317235-40.
• 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

50
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

51
ColloidsSummary

• There is NO evidence that colloids decrease
  mortality in the resuscitation of critically ill
  patients.

52
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 5-10 min

53
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 (6dextran) decreased mortality in 7/8
  trials overall 3.5 trend only ---gt Not stat
  sign

54
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

55
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

56
Hypertonic SalineConclusions

• 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..

57
Hemorrhagic Shock

• When to give fluids?
• How much?
• How fast?

58
Controlled Fluid ResuscitationRationale

• 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

59
Controlled Fluid ResuscitationEvidence

• Early animal 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)

60
Controlled Fluid ResuscitationEvidence

• Review articles
• Emerg Med Clinics 123(4). Nov 2002
• Journal of Trauma supplement Vol 54(5S). May 2003.

61
Bickell et al and Controlled Fluid Resuscitation
- here piggy,piggy
62
Bickell et al 1990The Detrimental Effects of
Intravenous Crystalloid after Aortotomy in Swine.
Surgery 110 529-36.

• 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

63
Bickell et al. NEJM 1994.Immediate versus
Delayed Fluid Resuscitation for Hypotensive
Patients with Penetrating Torso Trauma

• Study 598 patients SBPlt90, odd/even day
  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

64
Controlled Fluid ResuscitationWhat 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 -gt MAJOR protocol
  violations

65
Controlled Fluid ResuscitationWhat 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

66
Controlled Fluid ResuscitationWhat about blunt
trauma?

• Dutton RP. J. Trauma 2002. Hypotensive
  Resuscitation During Active Hemorrhage Impact on
  in Hospital Mortality
• RCT, N40, target SBP gt70 or gt 100
• ½ penetrating and ½ blunt trauma
• No difference in survival
• Small study, heterogenous patients, low mortality
  

67
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

68
Controlled Fluid Resuscitation Take home messages

• Early, aggressive fluid resuscitation increases
  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

69
Where will trauma resuscitation be in 2010?

• My prediction small volume of hypertonic saline
  dextran for target SBP 90 and to OR ASAP!

70
Cardiogenic Shock
71
Cardiogenic shock

• Definition
• decreased cardiac output and evidence of tissue
  hypoxia in presence of adequate intravascular
  volume
• Criteria
• hypotension (SBP lt 90) x 30 min, or 30mmHG below
  baseline, cardiac index lt 2.2 L/min/m2, PCWP gt 15
  mmHg
• Rosens 4 out of 6 criteria for empiric shock
• Pathologically
• Will have lost 40 of myocardium

72
Cardiogenic Shock
73
Cardiogenic ShockApproach

• Stabilize the ABCs
• Identify etiology of cardiogenic shock
• Small fluid bolus (250cc)
• Dont be shy on fluids if RV infarct
• Ionotropic/vasopressor support
• Manage infarct

74
Cardiogenic shock Ionotropic 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 lt 70 after fluids
• Others
• Amrinone, milrinone

75
MI Cardiogenic shockHow 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?

76
MI Cardiogenic shockHow to manage the MI?

• Thrombolysis in cardiogenic shock
• GISSI (N280) 30day mortality
• streptokinase 70.1
• medical mx 69.6
• NO trial has shown reduction mortality with
  cardiogenic shock with thrombolysis alone

77
MI Cardiogenic shockHow 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

78
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
• End Point early revasc. Med Mx stats
• 30d mortality 46.7 56 p.11
• 6m mortality 50.3 63.1 p.027

79
Cardiogenic Shockthe 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

80
MI Cardiogenic shockHow to manage the MI?

• Conclusions .
• Patients with AMI complicated by cardiogenic
  shock, especially those lt 75yo, should undergo
  emergent revascularization (PTCA or CABG)

81
Anaphylactic Shock

• Youd better know this!
• Airway management
• Epinephrine
• Benadryl
• Fluids
• Steroids
• Racemic epinephrine and ventolin nebs
• Ranitidine
• Glucagon

82
Etiology of Adrenal Crisis

• Underlying Adrenal Insufficiency
• (Addisions and Chronic Steriods)

Acute Precipitant
Adrenal Crisis
83
Acute adrenal crisis?

• Underlying Adrenal insufficiency
• Addisons disease
• Chronic steroids
• No underlying Adrenal insufficiency
• Adrenal infarct or hemorrhage
• Pituitary infarct or hemorrhage

• Precipitants of Adrenal crisis
• Surgery
• Anesthesia
• Procedures
• Infection
• MI/CVA/PE
• Alcohol/drugs
• Hypothermia

84
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

85
Features of Adrenal Insufficiency
86
Adrenal Crisis

• Consider on the differential diagnosis of SHOCK
  NYD

87
Management of Adrenal Crisis

• Corticosteroid replacement
• Dexamethasone 4mg iv q6hr is the drug of choice
  (doesnt 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

88
Conclusions

• Shock is the transition between illness and death
• Shock has many different causes but the end
  result is the same
• The differential diagnosis and management of
  shock is essential knowledge in emergency medicine

89
Collapse at triage

• 40 yo female, mentally challenged
• Collapses at triage No history available
• Looks shocky, altered LOC, HR 130, BP 70 palp,
  Sats 88, RR 30, C/S 7, Temp 38.2
• General exam no focal neuro abnormality, neck
  supple, pelvic normal, abdo soft but ? Diffuse
  tenderness, chest clear, ? Flow murmur, no signs
  of endocarditis
• Old chart 3 weeks post dc (day surgery) RA
• Pharmacy print out steroid Rx (?for arthritis)
• Wbc 20, pH 7.2, lactate 5, ECG sinus tach, CXR
  clear, urine dip clear

90
Case 1

• 23 yo female, CC collapsed with abdominal pain
  at wedding
• VS at triage BP 110/70, pulse 84, in mild
  distress
• 1 hour later physician assessment
• Anxious, clammy, BP 70/50, pulse 90
• ? Additional history
• ? Investigations
• ? Management

91
Case 2

• 88yo male CC chills, fever, malaise with triage
  vitals BP 130/94, HR 110 T38.6
• PMHx Afib, MI, CHF, HTN, COPD, dementia
• Multiple CV meds including warfarin
• W/u wbcs in urine, normal CXR, unchanged ECG,
  enlarged nontender prostate, stool OB ve, WBC 18
• 2hrs later BP drops to 85 systolic, pulse 120
• Ddx
• Management

92
Case 3

• You are called STAT to front door of ED to assist
  in extrication of patient from a car
• You find a young man who is pale, opens eyes to
  command, but has only thready rapid carotid
  pulse. Chest is clear.
• The driver says pt. Felt sick while eating a
  salad in a restaurant and asked to be driven to
  the hospital
• Ddx
• Mx