Ent and head neck surgery

1. Shock and SIRS
Dr. Subash Bhatta
1st Year, MS (ORL-HNS)
GMSMA of ENT-HN Studies
MMC-TUTH, IOM

2. Roadmap
Definition
Historical overview
Brief introduction
Pathophysiology
Stages
Classification
Hypovolemic shock
Cardiogenic shock
Obstructive shock
Distributive shock
Septic shock and SIRS
Neurogenic shock
Anaphylactic shock

3. Shock
Definition
 It is a condition produced by inability of the circulatory system to adequately nourish tissues or
remove toxic metabolites.
 It is a condition of profound hemodynamic and metabolic disturbance characterized by failure
of the circulatory system to maintain an appropriate blood supply to the microcirculation with
consequent inadequate perfusion of vital organs.
 An acute medical condition associated with a fall in blood pressure, caused by such events as
loss of blood, severe burns, allergic reaction, or sudden emotional stress, and marked by
cold, pallid skin, irregular breathing, rapid pulse, and dilated pupils.
Emergency medicine by Rosen and Barkin 4th edition
Rubins pathology 4th edition
Oxford dictionary

4. Shock definition contd..
 A condition of acute peripheral circulatory failure due to derangement of circulatory control
or loss of circulating fluid, marked by hypotension
and coldness of the skin, and often by tachycardia and anxiety if untreated cab be fatal.
 A life threatening medical condition of low blood perfusion to tissues resulting in cellular
injury and inadequate tissue function , typical signs being low blood pressure, rapid heart
rate, and signs of poor end-organ perfusion.
Wikipedia
Dorland medical dictionary

5. History
 First resuscitation efforts by Ambroise Pare
back in 1510 to 1590
 Treatment of shock started back in Dec14, 1650, By Dr. William(king,s doctor,
England) unknowningly revived a person declared dead after judicial hanging.

6. History contd..
 First intravenous fluid therapy in 1830 by Herman for cholera
 Gross was the first to define the shock as
 Manifestation of a “rude unhinging of the machinery of life”
 Crile was the first to do blood transfusion on 1900
 Later Alexis Carrel went on to study about blood group

7. Introduction
 Most common & most important cause of death among surgical patients.
 Death may be immediate as a result of profound shock or delayed due do organ ischemia or
reperfusion injury.
 Shock is not a disease itself, its constellations of manifestations of various diseases and
conditions.
Sabiston textbook of surgery 17th ed
“Transitions between a illness and death”

8. Introduction
Most common cause of shock in Nepal is RTA.
The recent earthquake was the major cause of the patient with shock in various part of the country
Total death 7619
Total injured 14,454 Source: Nepal Police:www.nepalpolice.gov.np

9. Pathophysiology
Circulatory system four part machine
 Pump (the heart)
 A complex system of flexible tubes
(the blood vessels)
 A circulating fluid (the blood)
 Fine regulating system or “computer” (the nervous system)

10. Pathophysiology contd..
Pic source internet

11. Pathophysiology contd..

12. Pathophysiology contd..
Enters vicious cycle
Hypoxia
Increased vascular
permeability
Loss of total blood
volume
Decreased blood to
myocardium
Myocardial injury
Myocardial injury
Reduced CO
Reduced renal perfusion
Reduced clearance of
products
Acidosis
-ve ionotrophic
Respiratory distress
Aggravates shock
Ion homeostasis
Cell structure
Electrical and mechanical fxn
alters
Hypoxia
Not managed
Cycle continues with more
severity

13. Pathophysiology contd..
Various organ response
 Cellular level
 Aerobic to anaerobic cycle-lactic acid
 Disruption of cell membrane end stage in
all form of shock
Metabolic acidosis
Tinnitus,vertigo.
Visual disturbances
Palpitations
Chest pain
arrythmias
Cranial nerve palsies
Headache
Lethargy, stupor, and
coma
Mental confusion
Dyspnea
Hyperventilation
Kussmaul respiration
Nausea and vomiting
Abdominal pain
Diarrhea
Polyphagia
Generalized muscle
weakness
Bone pain
Increased
intracellular Ca
Electric pump failure
Increased
intracellular Na
Hypo calcemia Apoptosis

14. Various organ response contd
 Micro vascular
 Activation of complement and prime neutrophil
 Endothelial injury, increased permeability
Edema Anasarca
Systemic
Cardiovascular
Tachycardia
Low BP
Respiratory
Increased rate
Shallow breathing
Renal
Decreased urine
output
Endocrinological
Release of
catecholamine

15. Various organ response contd…
 Ischemia reperfusion injury
Local inflammatory mediators get disseminated with increase in perfusion.
• Myocardial depression
• Vascular dilatation
• Endothelial injury in kidney and
lungs
Cause of delayed death after resuscitation in shock

16. Stages
Stage I
compensated, or nonprogressive
Stage II
decompensated, or progressive
Stage III
irreversible
Fast heart rate
Vasoconstriction
Slight decreased UO
Treatment completely halt
progression
Compensatory methods begins
to fail
Symptoms more
prominent
Symptoms can be
reversed
Permanent damage
done
Heart failure
Renal shutdown
CNS dysfunction
Cant be
revived
Death
Mild
Moderate
Severe

17. Stages with clinical manifestations
Parameters/
stages
Compensated Mild Moderate Severe
Lactic acidosis + ++ +++ ++++
Urine output Normal Normal Reduced(<0.5ml/kg
/hr)
Anuric
Consciousness
level
Normal Mild anxiety Drowsy Comatose
Respiratory rate Normal Increased(>20 upto
30/minutes in
adults)
>30/minutes Shallow and labored
Pulse rate 80-100/min 100-130/min >130/min >130/min or not
detected
Blood pressure Normal Normal Mild hypotension Severe hypotension
Short practice of baily and love 25th edi

18. Stages with clinical manifestations various pitfalls
Capillary refill
Tachycardia
Blood pressure
Central venous pressure
Hematocrit or
hemoglobulin level
So much variation
No fixed universal value
Can lead to

19. Classification
First time in ninetienth century
Cardiac cause
Brain dysfunction
Due to microorganisms
Due to blood loss

20. Classification contd..
Emergency medicine by rosen and barkin 4th edi
Qualitative
Quantitative
Shock Hemorrhage
Myocardial dyfxn
Circulatory obstructiom
hypovolemia
AV fistula
Sepsis
Anaphylaxis
dyshemoglubunemia
Heat shock
hypothermia

21. Classification contd..
Hypovolemic
Cardiogenic
Distributive
Obstructive
Bailey and Love 25th edi

22. Hypovolemic shock
 Most common
 Shock is hypovolemic until diagnosed otherwise
 Some degree of component of all form of shock
Hypovolemia
Hypo
Volume
Reduction
Body fluid
Reduction in body fluid

23. Hypovolemic shock contd
Definition
Hypovolemic shock refers to a medical or surgical condition in which rapid fluid loss results in
multiple organ failure due to inadequate circulating volume and subsequent inadequate perfusion.
Vicious triad

24. Hypovolemic shock contd
Total body fluid
Intracellular fluid
40%
Extracellular fluid
60%
Interstitial
20%
Plasma
40%
60% of total
body weight
Circulating blood
Loss, main cause of hypovolemia

25. Hypovolemic shock etiology
Causes
Hemorrhage
Hemorrhage
Hemorrhage
1st, 2nd and 3rd
Internal External
RTA causig solid organ injury
liver,spleen,lungs,GI tract
Ulcers in GI tract
Esophageal varices
Dissection of aorta
Hemoptysis
Bronchogenic Ca
Intra bronchial TB
RTA
Trauma due to any cause
Gynaecological and obstetrics cause
most common in Nepalese women
Intraoperative bleeding
ENT causes
Bleeding diathesis
DIC
Blood on the floor, plus 4 more" = intrathoracic, intraperitoneal, retroperitoneal, pelvis/thigh

26. Hypovolemic shock etiology contd
 ENT bleeding producing shock
Epistaxis
Post tonsillectomy hemorrhage
Intra and post operative bleedings
Traumatic ENT bleedings

27. Hypovolemic shock etiology contd
Causes other than hemorrhage
Diarrhoea and vomiting
Burns
All kinds of burns
Small bowel obstructions
Hours of hyperglycemia (DKA)
Tension pneumothorax
Anaphylactic shock
Fluid discharging lesions
Dermal conditions

28. Hypovolemic shock stages
Stages of hemorrhage
Stage 1(<15%, 750ml approximately)
BP maintained
Normal respiratory rate(12-20/min)
Skin pale
Normal mental status to slight anxiety
Normal capillary refill
Normal urine output
Stage 2(15-30%, 750-1500ml approximately)
Systolic blood pressure maintained
Increased diastolic blood pressure
Narrow pulse pressure
Tachycardia >100bpm
Tachypnoea>20/min
Pale, cold, and clammy skin
Mildly anxious/Restless
Delayed capillary refill>2sec
Urine output 20-30 ml/hour

29. Hypovolemic shock stages contd
Stages of hemorrhage
Stage 3(30-40%, 1500-2000ml
approximately)
Systolic BP 100mmHg or less
Marked tachycardia >120 bpm
Marked tachypnea>30/min
Confusion, anxiety, agitation
Sweating, cool, pale skin
Delayed capillary refill >3sec
Urine output 20 ml/hour
Stage 4(>40%, >2000ml approximately)
Tachycardia >140
Shallow respiration
Systolic blood pressure of 70 mmHg or less
Decreased consciousness, lethargy, coma
Skin sweaty, cool, and extremely pale (moribund)
Absent capillary refill
Negligible urine output
Survival is extremely unlikely

30. Hypovolemic shock contd
Other clinical manifestations
Vague symptoms like
 Lethargy
 Weakness
 Drowsiness
 Nausea,vomiting
 Abdominal pain
 Chest pain
 Difficult in respiration

31. Hypovolemic shock management
Management algorithym
Resuscitation
History, clinical examination and
investigations
simultaneously
ABC
To find out
The type of shock
Doubt
In the line of hypovolemic
shock without delay
Look for response
Control of bleeder
May require OT
Done in ER
With help of
i.v. fluid therapy only after
bleeding has stopped

32. Hypovolemic shock management contd
i.v. fluid therapy
Responders Transient Responders
Non Responders
When and how to administer the fluid
Crystalloid Colloid Blood
Best to replace the blood
loss
No O2 carrying capacity
Hartman solution
NS
RL
albumin

33. Hypovolemic shock management contd
 Long term critical care management and treat the primary.
Use of vasopressors
Phenylephrine
Dobutamine
adrenaline
Never be used as primary method in hypovolemic shock
Only when heart has something to pump i.e after fluid therapy
Don’t flog the tired horse
Monitoring
Heart rate
Noninvasive BP
SPO2
Hourly UO
ECG
More invasive like
CVP
Cardiac output
Systemic vascular resistance
Preload
Serious pts
Systemic and Organ
perfusion monitoring

34. Hypovolemic shock contd
Systemic and Organ perfusion monitoring
Urine output
Level of conscious
Base deficit/lactic acidosis
Mixed venous oxygen saturation
Less reliable
More reliable
End point in resusucitation
Easily known when to start but slight difficult to decide when to stop
Previously used
Pulse
BP
Consciousness level
Urine output
Not that reliable
Base deficit
Mixed venous oxygen
saturation
Lactate

35. Obstructive shock
Definition
Form of shock associated with physical obstruction of the great vessels or the heart
itself causing the decreased blood supply and various manifestation leading
progressively to multi-organ failure and ultimately death if not dealt properly.
Pulmonary embolism
Cardiac tamponade
Tension pneumothorax
Most common causes

36. Obstructive shock
Obstructive shock has much in common with cardiogenic shock, and the two are
frequently grouped together.
Some sources do not recognize obstructive shock as a distinct category,
and categorize pulmonary embolism and cardiac tamponade under
cardiogenic shock.
Except for management of the underlying individual pathology the obstructive shock is similar to
cardiogenic shock
wikipedia
Sabiston textbook of surgery 17th ed

37. Cardiogenic shock
Life-threatening medical condition resulting from an
inadequate circulation of blood due to primary failure of
the ventricles of the heart to function effectively
Characterized by systemic hypo perfusion due to severe
depression of the cardiac index [<2.2 (L/min)/m2] and
sustained systolic arterial hypotension (<90 mmHg) despite
an elevated filling pressure [pulmonary capillary wedge
pressure (PCWP) >18 mmHg].
 Ciculatory shock
 Insufficient perfusion of tissue to meet the demands for oxygen and nutrients

38. Cardiogenic shock contd
 Highest mortality rate, 80% mortality
 More common in elderly
 More in patients with other comorbidities
 More in patients with STEMI
 Common in 2nd episode of STEMI
 Common in patients with some intervention in the past
 LV failure accounts for ~80% of cases of CS complicating acute MI
 Leading cause of death of patients hospitalized with MI

39. Cardiogenic shock etiology
 Acute myocardial infarction/ischemia
 LV failure
 Papillary muscle/chordal rupture—severe MR
 Ventricular free wall rupture with sub acute tamponade
 Hemorrhage
 Excess negative inotropic or vasodilator medications
 Prior valvular heart disease
 Post-cardiac arrest
 Post-cardiotomy
 Refractory sustained tachyarrhythmias
 Acute fulminant myocarditis
 End-stage cardiomyopathy
Most common

40. Cardiogenic shock etiology contd
 Left ventricular apical ballooning
 Hypertrophic cardiomyopathy with severe outflow obstruction
 Aortic dissection with aortic insufficiency or tamponade
 Pulmonary embolus
 Severe valvular heart disease
 Critical aortic or mitral stenosis
 Acute severe aortic or mitral regurgitation
 Toxic-metabolic
 Beta-blocker or calcium channel antagonist overdose

41. Cardiogenic shock pathophysiology

42. Cardiogenic shock contd
Those at Special risk
 Acute MI
 Older age
 Female sex
 Prior MI
 Diabetes
 Anterior MI location
 Reinfarction soon after MI

43. Cardiogenic shock clinical signs and symptoms
 Continuing chest pain and dyspnea
 Appear pale, apprehensive, and diaphoretic
 Mentation altered, with somnolence, confusion, and agitation
 Pulse is typically weak and rapid (90–110 beats/min) or
severe bradycardia due to high-grade heart block may be present

44. Cardiogenic shock clinical signs and symptoms contd
 Systolic blood pressure reduced (<90 mmHg) with a narrow pulse pressure (<30
mmHg)
 Tachypnea, Cheyne-Stokes respirations, and jugular venous distention may be
present
 Precordium typically quiet, with a weak apical pulse
S1 soft and an S3 gallop may be audible, systolic murmurs, Rales audible
 Oliguria (urine output <30 mL/h) is common.

45. Cardiogenic shock management algorithym
Treat the arrythmia

46. Laboratory Findings
 TLC elevated, left shift
 RFT initially normal, but BUN and creatinine rise progressively
 LFT deranged
 Anion-gap acidosis with elevation of the lactic acid level
 Cardiac markers markedly elevated
Electrocardiogram
 Q waves and/or >2-mm ST elevation in multiple leads or left bundle branch block
 More than one-half of all infarcts associated with shock are anterior
 Global ischemia due to severe left main stenosis usually is accompanied by severe (e.g.,
>3 mm) ST depressions in multiple leads.
Cardiogenic shock management algorithym contd

47. Cardiogenic shock management algorithym contd
Chest Roentgenogram
 Pulmonary vascular congestion
 Pulmonary edema
 Heart size normal when CS results from a first MI but enlarged with a previous MI.
Echocardiogram
 Left-to-right shunt
 Proximal aortic dissection with aortic regurgitation or tamponade
 Pulmonary embolism

48. Distributive shock
Medical condition in which abnormal distribution of blood flow in the smallest blood vessels
results in inadequate supply of blood to the body's tissues and organs.
Types
Septic shock most common
Neurogenic shock
Anaphylactic shock
Blood
accumulates

49. Septic shock & SIRS
SIRS stand for “Systemic Inflammatory response syndrome”
Definition
An exaggerated and generalized manifestation of a local
immune or inflammatory reaction and is often fatal.
Hyper metabolic state with two or more sign of systemic inflammation, such as
fever, tachycardia, leukocytosis or leukopenia in a setting of known cause of
inflammation.
An inflammatory state affecting the whole body, frequently a response of the
immune system to infection, but not necessarily so, sometimes can be non-
infectious.
Rubin’s pathology 4th edi
Harrisson’s medicine 18th edi
Wikipedia

50. Septic shock & SIRS
Local response
Systemic response
rubor
calor
tumor
dolor
Functionolesia
Fever or hypothermia
Leukocytosis or leukocytopenia
Tachycardia or bradycardia
Systemic Inflammatory response syndrome
Infectious Non infectious
Mostly

51. Septic shock & SIRS
Systemic Inflammatory response syndrome + Infection
Sepsis
Dysfunction of organ in the site distant from the site of
infection with hypotension and hypo perfusion.
Severe Sepsis
+
Hypotension and Hypo perfusion not corrected with fluid
infusion for at least 1 h despite adequate fluid
resuscitation
Septic shock
By consensus conference committee in 1992 and revised in 2001
+

52. Septic shock & SIRS
Criteria of SIRS
Fever
more than 38°C (100.4°F) or
less than 36°C (96.8°F)
Heart rate
more than 90 beats per minute
Respiratory rate
Less than 20 breaths per minute or
Arterial carbon dioxide tension (PaCO 2) of less than 32 mm Hg
Abnormal white blood cell count
>12,000/µL or
< 4,000/µL or
>10% immature band forms
SIRS can be diagnosed when two or more of these criteria are present

53. Septic shock & SIRS
Epidemiology
 Increase in incidence for last decade
Good diagnostic facility
Longevity of life among chronically diseased persons
Wide spread use of
 immunosuppressive drugs
 indwelling catheters
 mechanical devices
 More in elderly and children
 No sex preponderance(M=F)
Female more in developing countries due to Gynae/Obstetrics problems
 More in patients with chronic illness
AIDS, DM, CKD

54. Septic shock & SIRS
Some terms of special mention
Bacteremia
Presence of bacteria in blood, as evidenced by positive blood cultures
Septicemia
Presence of microbes or their toxins in blood
Refractory septic shock
Septic shock that lasts for >1 h and does not respond to fluid or pressor administration
Multiple-organ dysfunction syndrome (MODS)
Dysfunction of more than one organ, requiring intervention to maintain homeostasis

55. Septic shock & SIRS etiology
 Ischemia
 hemorrhage
 Complications of surgery
 Adrenal insufficiency
 Pulmonary embolism
 Complicated aortic aneurysm
 Cardiac tamponade
 Anaphylaxis
 Drug overdose
NON INFECTIOUS

56. Septic shock & SIRS etiology contd

57. Septic shock & SIRS
20-40% of cases of severe sepsis
40-70% cases of septic shock Blood culture positive
Approx. 80%
Bacterial
Fungi
Mixture of other microbes

58. Septic shock & SIRS pathophysiology
Most cases triggered by bacteria or fungi not causing systemic disease in immunocompetent hosts
Some microbial pathogens, in contrast, can circumvent innate defenses because
(1) lack molecules that can be recognized by host receptors
(2) elaborate toxins or other virulence factors
In both cases, the body can mount a vigorous inflammatory reaction resulting in severe sepsis yet
fails to kill the invaders
Septic response may also be induced by microbial exotoxins that act as superantigens (e.g., toxic
shock syndrome toxin 1) as well as by many pathogenic viruses.

59. Septic shock & SIRS pathophysiology
Bacterial
products
CD14 TLR

60. Septic shock & SIRS clinical presentations
How the patient presents?
In shock patient don’t present, rather he is presented by others.
S
E
P
S
I
S
Shivering, fever or very cold
Extreme pain and generalized discomfort
Pale or discolored skin
Sleepy, difficult to rouse, confused
“I feel I might die” feeling of impending doom
Shortness of breath

61. Septic shock & SIRS clinical presentations contd
 Superimposed on the symptoms and signs of the patient's underlying
illness and primary infection.
 Rate at which severe sepsis develops may differ from patient to patient.
some may be normo or hypothermic
absence of fever most common
in neonates
in elderly patients
in persons with uremia or alcoholism.

62. Septic shock & SIRS clinical presentations contd
 Hyperventilation
 Acrocyanosis and ischemic necrosis of digits
 Cellulitis, Pustules, bullae, or hemorrhagic lesions

63. Septic shock & SIRS clinical presentations contd
Skin lesions may suggest specific pathogens occasionally
Sepsis with cutaneous petechiae or purpura then N. meningitidis (or, less
commonly, H. influenzae)
Patient bitten by a tick endemic area, petechial lesions suggest Rocky
Mountain spotted fever
Cutaneous bullous lesion, surrounded by edema, that undergoes central
hemorrhage and necrosis almost exclusively in neutropenic patients is ecthyma
gangrenosum, caused by P. aeruginosa.
Hemorrhagic or bullous lesions with h/o eating raw oysters suggest V.
vulnificus bacteremia
Generalized erythroderma in a septic patient suggests the toxic shock
syndrome due to S. aureus or S. pyogenes.

64. Septic shock & SIRS clinical presentations contd
Gastrointestinal manifestations
 Nausea, vomiting, diarrhea, and ileus
 Stress ulceration can lead to upper GI bleeding
 Cholestatic jaundice
 Hepatocellular or canalicular dysfunction

65. Septic shock & SIRS major complications
Cardiopulmonary Complications
 Acute lung injury or ARDS in 50% cases
 Respiratory muscle fatigue hypoxemia and hypercapnia elevated pulmonary
capillary wedge pressure (>18 mmHg) volume overload or cardiac failure
 Pneumonia caused by viruses or by Pneumocystis
 Sepsis-induced hypotension refractory hypotension
 Depression of myocardial function
 Death results from refractory shock or the failure of multiple organs rather than from
cardiac dysfunction per se.

66. Septic shock & SIRS major complications contd
Adrenal Insufficiency
 Plasma cortisol level of <15mcg/mL
 Hypotension that is refractory to fluid replacement and requires pressor therapy
Renal Complications
 Oliguria
 Azotemia
 Proteinuria
 Nonspecific urinary casts
 Acute tubular necrosis
 Glomerulonephritis
 Renal cortical necrosis
 Interstitial nephritis

67. Septic shock & SIRS major complications
Coagulopathy
 Platelet counts are usually very low (<50,000/microL)
 DIC
Immunosuppression
Neurologic Complications
 Polyneuropathy
 Guillain-barré syndrome
 Motor weakness

68. Septic shock & SIRS management
Investigations
Blood investigations
Leukocytosis or Leukopenia
Thrombocytopenia becoming more severe with advanced disease
Neutrophils may contain toxic granulations, Döhle bodies, or cytoplasmic vacuoles
Prolongation of the thrombin time
Decreased fibrinogen
The presence of d-dimers
Azotemia
LFT deranged
Active hemolysis suggests clostridial bacteremia, malaria, a drug reaction, or DIC
DIC
In the case of DIC, microangiopathic changes may be seen on a blood smear

69. Septic shock & SIRS management contd
Arterial blood gas
Respiratory alkalosis due to hyper ventilation
Metabolic acidosis (with increased anion gap) typically supervenes
Hypoxemia initially correctable with supplemental oxygen, if refractoriness to 100% oxygen
indicates right-to-left shunting
Chest radiograph
May be normal
May show evidence of
Underlying pneumonia
Volume overload
Diffuse infiltrates of ARDS
Electrocardiogram
sinus tachycardia
nonspecific ST–T-wave abnormalities.

70. Septic shock & SIRS management contd
Sugar profile
Hyperglycemia
Hypoglycemia occurs rarely
Severe infection may precipitate diabetic ketoacidosis that may exacerbate hypotension
Serum albumin level declines as sepsis continues
Hypocalcemia rare
Urine R/E
Hematuria
Proteinuria
Pus cells

71. Septic shock & SIRS management contd
Diagnosis
No specific diagnostic test
Diagnostically sensitive findings
Fever or hypothermia
Tachypnea or tachycardia
Leukocytosis or leukopenia
Acutely altered mental status
Thrombocytopenia
An elevated blood lactate level
Hypotension

72. Septic shock & SIRS management contd
Quite variable manifestation
In one study(PGI chandigarh)
33% had a normal temperature
44% had a normal respiratory rate
14% had a normal pulse rate
38% had normal white blood cell counts.
Systemic responses of uninfected patients with other conditions may be similar to those
characteristic of sepsis.

73. Septic shock & SIRS management contd
Definitive etiologic diagnosis
Culture
Blood
Local infection
site
Two blood samples
From two different venipuncture sites
Patient with an indwelling catheter
one sample from each lumen and
another via venipuncture
Many negative
Antibiotic administration
Slow-growing or fastidious organisms
Absence of microbial
invasion
Gram staining
Polymerase
chain reaction
To identify microbial DNA in peripheral-
blood or tissue samples
Definitive
Sometimes

74. Septic shock & SIRS management contd
Examine skin and mucosa for lesions that might yield diagnostic information as described earlier.
With overwhelming bacteremia
Pneumococcal sepsis in splenectomized individuals
Fulminant meningococcemia
Infection with V. Vulnificus, B. Pseudomallei, or Y. Pestis
Microorganisms are sometimes
visible on buffy coat smears of
peripheral blood.

75. Septic shock & SIRS management
Personnel who are experienced in the care of the critically ill
Urgent measures to treat the infection
To provide hemodynamic and respiratory support
To eliminate the offending microorganisms
These measures should be initiated within 1 hour of the patient's presentation
Rapid assessment and diagnosis are very essential

76. Septic shock & SIRS management contd
Antimicobials Resuscitation
Hemodynamic, Respiratory,
and Metabolic Support
Removal of infection source
Simultaneously
General support

77. Septic shock & SIRS management contd
 Anti microbial agents
 Immunocompetent
Piperacillin-tazobactam (3.375 g q4–6h)
Imipenem-cilastatin (0.5 g q6h)
Meropenem (1 g q8h)
Cefepime (2 g q12h)
If allergic to lactam agents
Ciprofloxacin (400 mg q12h)
Levofloxacin (500–750 mg q12h) plus clindamycin (600 mg q8h)
Vancomycin (15 mg/kg q12h) should be added to each of the above regimens

78. Septic shock & SIRS management contd
 Neutropenic (<500 neutrophils/L)
Imipenem-cilastatin (0.5 g q6h) or Meropenem (1 g q8h) or Cefepime (2 g q8h)
Piperacillin tazobactam (3.375 g q4h) plus tobramycin (5–7 mg/kg q24h)
Vancomycin (15 mg/kg q12h) should be added if
indwelling vascular catheter
has received quinolone prophylaxis
has received intensive chemotherapy that produces mucosal damage
Staphylococci are suspected
Empirical antifungal therapy with an echinocandin or amphotericin B

79. Septic shock & SIRS management contd
 IV drug user
Vancomycin (15 mg/kg q12h)
 AIDS
Cefepime (2 g q8h) or piperacillin-tazobactam (3.375 g q4h) plus tobramycin (5–7 mg/kg q24h)
If the patient is allergic to lactam drugs
Ciprofloxacin (400 mg q12h) or levofloxacin (750 mg q12h)
plus vancomycin (15 mg/kg q12h) plus tobramycin
 Splenectomy
Cefotaxime (2 g q6–8h) or ceftriaxone (2 g q12h)
Add vancomycin, If local prevalence of cephalosporin-resistant pneumococci high
Patient allergic to lactam drugs
vancomycin (15 mg/kg q12h) plus either moxifloxacin (400 mg q24h)
or levofloxacin (750 mg q24h) or aztreonam (2 g q8h)

80. Septic shock & SIRS management
 Removal of the Source of Infection
Drainage of a focal source of infection is essential
lungs, abdomen and urinary tract
Foley and drainage catheters should be replaced
Indwelling IV or arterial catheters removed
Tip rolled over a blood agar plate for culture
New catheter should be inserted at a different site after initiation of antibiotic therapy
The possibility of paranasal sinusitis for patient with nasal intubation.

81. Septic shock & SIRS management
 Hemodynamic, Respiratory, and Metabolic Support
Primary goals
 to restore adequate oxygen and substrate delivery to the tissues
 to improve tissue oxygen utilization and cellular metabolism
 to make adequate organ perfusion, restore circulation
 General Support
 Nutritional supplementation by enteral delivery route
 Prophylactic heparinization to prevent deep venous thrombosis
 Prevention of skin breakdown, nosocomial infections, and stress ulcers.
 Tight control of the blood glucose concentration

82. Septic shock & SIRS management
 Prognosis
20–35% of patients with severe sepsis and 40–60% of patients with septic shock die within 30
days, Others die within the ensuing 6 months.
Late deaths
poorly controlled infection
immunosuppression
complications of intensive care
failure of multiple organs
the patient's underlying disease
Case-fatality rates similar for culture-positive and culture-negative severe sepsis
With no known preexisting morbidity
Case-fatality rate <10% until 40 years of age, increases to exceed 35% in the very elderly
Death is significantly more likely in severely septic patients with preexisting illness

83. Septic shock & SIRS management
Prevention
 Best to reduce morbidity and mortality
 Most cases complications of nosocomial infections
 Reducing the number of invasive procedures undertaken
 Limiting the use (and duration of use) of indwelling vascular and bladder catheters
 Reducing incidence and duration of profound neutropenia (<500 neutrophils/L)
 Aggressively treating localized nosocomial infections
 Avoid indiscriminate use of antimicrobial agents and glucocorticoids

84. Neurogenic shock
Distributive type of shock resulting in low blood pressure, occasionally with a slowed heart rate,
that is attributed to the disruption of the autonomic pathways within the spinal cord.
Low blood pressure due to decreased systemic vascular resistance results in pooling of blood
within the extremities lacking sympathetic tone.
The slowed heart rate results from unopposed
vagal activity and has been found to be exacerbated
by hypoxia and endo bronchial suction.

85. Neurogenic shock
Peripheral pooling of blood makes less blood available for tissue perfusion,
decreased venous return causing decreased cardiac output.
Neurogenic shock can be a potentially devastating complication, leading to organ
dysfunction and death if not promptly recognized and treated
It is not to be confused with spinal shock, which is not circulatory in nature.

86. Neurogenic shock etiology
 Blunt or penetrating trauma/injury to the spinal cord
Rotation, dislocation, over- flexion/extension of the spinal cord.
Motor vehicle accidents
Sports injuries
Falls, stab and gunshot wounds.
 Improper administration of regional anesthesia
 Drugs and medications which affect the autonomic nervous system can also cause neurogenic
shock

87. Neurogenic shock clinical signs and symptoms
 Hypotension
 Bradycardia
 Hypothermia
 Difficulty in breathing and has rapid and deep shallow breathing.
 The skin feels warm to touch in contrast to hypovolemic and cardiogenic
 Facial pallor
 Dizziness, lightheadedness, fainting
 Nausea and vomiting

88. Neurogenic shock clinical signs and symptoms
 Faint and rapid pulse.
 Patient experiences weakness due to insufficient blood supply.
 Patient stares blankly at nothing.
 Feels anxious and there can be changes in mental state or disorientation.
 Does not respond to any stimuli.
 Has bluish discoloration of lips and fingers (cyanosis).
 Decreased or absent urine output.
 Sweats profusely.
 Considerable chest pain.
 Loss of consciousness.

89. Neurogenic shock diagnosis
Complete physical examination and medical history
Key to the diagnosis
Various tests
Blood
Urine tests
Imaging
CT scan
MRI scan
X-rays
Ultrasound
Carried out to assess the patient's medical condition and the extent of injury or damage.

90. Neurogenic shock management protocol
Assessment of general condition
Stabilize the patient and prevent any irreversible tissue damage including revival of the patient
Simultaneus resuscitation
Airway pattern
Breathing including the circulation
Spinal immobilization is must
Arterial blood pressure, through administration of IV fluids to restore the mean pressure
Inotrophics
Dopamine
Dobutamine
Other inotropic agents may be infused in case of inadequate fluid resuscitation

91. Neurogenic shock management protocol
Severe bradycardia
IV infusion of atropine given 0.5mg to 1 mg every 5 minutes for a total dosage of 3.0 mg
a pacemaker if necessary
High dosage of methylprednisolone within 8 hours following the onset of neurogenic shock in
cases where neurological deficit has already been present.
Vitals stable
Immediately transfer the patient to neuro tertiary unit for definitive
management to prevent the permanent neurological deficit
Rehabilitation of the patients
who have permanent disability

92. Anaphylactic shock
A widespread and very serious allergic reaction with symptoms including dizziness, loss of
consciousness, labored breathing, swelling of the tongue and breathing tubes, blueness of the
skin, low blood pressure, heart failure, and death.
Is a systemic, type I hypersensitivity reaction that often has fatal consequences.
Caused by a runaway histamine response to an allergic reaction
Foreign matter of any type penetrates
the skin, mucous membranes, or digestive system
histamine
Increased blood to affected
area
Swelling from edema and
inflammation
Restricts blood flow to the
affected area
Protective action
Mosquito bite
Bee sting
Normally

93. Anaphylactic shock
In some individuals the histamine response is triggered by substances that are not inherently
harmful to the human body
Normal histamine response is atypically aggressive
Causing the normal symptoms associated with a histamine response to be somewhat more severe
Allergy Mostly it is only annoying not distressing
In some causes acutely distressing symptoms
Anaphylacsis
Anaphylactic shock

94. Anaphylactic shock causes

95. Anaphylactic shock pathophysiology

96. Anaphylactic shock signs and symptoms

97. Anaphylactic shock management algorithm

98. References
 Harrison's Principles of Internal Medicine 18th Ed
 Short practice of baily and love 25th edition
 Pathology basis of diseases, Robbins and Cotran 7th edi and 8th edi
 Rubins pathology 4th edition
 Emergency medicine by Rosen and Barkin 4th edition
 Sabiston textbook of surgery 17th ed
 Textbook of medical physiology guyton and hall 11th edi
 Scott Brown 7th edition Otorhinolaryngology, Head & Neck Surgery
 Internet (www.google.com)
 Wikipedia
 Medscape