Diagnosis, Investigations and Management of Shock

1. DIAGNOSIS, INVESTIGATIONS
AND
MANAGEMENT OF SHOCK

2. CONTENTS
 Introduction
 Classification of shock
 Hypovolaemic shock
 Introduction
 Etiology
 Clinical Features
 Treatment Principles
 Treatment
 Cardiogenic Shock
 Etiology
 Investigations
 Management
 Septic Shock
 Introduction
 Etiology
 Stages of Septic Shock
 Investigations
 Treatment
 Neurogenic Shock
 Introduction
 Etiology
 Clinical features
 Management
 Endocrine Shock
 Etiology
 Anaphylactic Shock
 Introduction
 Clinical Features
 Treatment
 Severity Of Shock
 Mild Shock
 Moderate Shock
 Severe Shock

3. CONTENTS
 Effects of Shock on various organs
 Heart
 Lung
 Metabolic
 Cellular changes
 Brain
 Kidneys
 Blood
 Gastro – intestinal Tract
 Multiple Organ Dysfunction
Syndrome
 Introduction
 Features related to MODS
 Management

4. SHOCK
A systemic state of low tissue perfusion which is
inadequate for normal cellular respiration.

5. Occurs due to circulatory
collapse and tissue hypoxia.
With insufficient delivery of oxygen and
glucose, cells switch from aerobic to anaerobic
metabolism causing lactic acidosis.
If perfusion is not restored in a timely fashion,
cell death occurs.
Intracellular potassium is released into
circulation.

6. Intracellular lysosomes break down and
release powerful enzymes which destroy
their own cells.
Hypoxia and acidosis through
complements release free oxygen
radicals and cytokines which damage
capillary endothelium.
Eventually cardiovascular, respiratory,
renal, endocrine and GIT will be affected
presenting as systemic features.

7. CLASSIFICATION OF SHOCK
HYPOVOLAEMI
C SHOCK
CARDIOGENIC
SHOCK
SEPTIC SHOCK
NEUROGENIC
SHOCK
RESPIRATORY
SHOCK
ANAPHYLACTIC
SHOCK
ENDOCRINE
SHOCK

9. HYPOVOLAEMIC
SHOCK
This is the most common type of shock out of all the
varieties encountered in the emergencies of the
hospitals.

10. ETIOLOGY
HAEMORRHAGE
• External from trauma,
open fractures
• Internal injury to spleen,
liver, mesentery
SEVERE BURNS
• Which result in loss of
plasma
Peritonitis, Intestinal
Obstruction
Diarrhoea and
vomiting due to any
cause

11. CLINICAL FEATURES
Rapid heart
beat
Quick
shallow
breathing
Feeling
weak, being
tired
Confusion,
altered
mental status
Low blood
pressure
Low urine
output
Cool,
clammy skin

12. TREATMENT PRINCIPLES
CONTROL ONGOING LOSS
RAPID RE-EXPANSION OF THE CIRCULATING
INTRAVASCULAR BLOOD VOLUME
+
GOAL : Restore blood volume & improve tissue
perfusion and oxygenation

13. TREATMENT
Oxygen therapy
Intravenous fluids including colloids and
crystalloids, including blood if required
Treat the cause

14. CARDIOGENIC
SHOCK
It is defined as circulatory failure causing diminished
forward flow of blood leading into tissue hypoxia with
systolic blood pressure less than 90mm of hg for 30
minutes and raised pulmonary capillary wedge pressure
(PCWP) more than 15mm of hg.

15. It is commonly seen in acute myocardial infarction (MI) with mortality
more than 50%.
Cardiogenic shock develops within 24 hours of MI.
It occurs when 50% of left ventricular wall is damaged by infarction.
It leads to pulmonary oedema and severe hypoxia.
Ischaemic necrosis of left ventricular wall causes failure of pump
thereby decreasing the stroke volume.

16. ETIOLOGY
Acute
Myocardial
Infarction
Acute
pulmonary
embolism
Acute
carditis
Drug
induced
Congenital
heart
disease
Toxaemia of
any cause
Cardiac
Temponade
Cardiac
surgical
conditions
Trauma to
heart

17. INVESTIGATIONS
Electro Cardio Gram (ECG)
Echocardiography
Arterial blood gas analysis
Cardiac enzymes
Pulmonary Capillary Wedge Pressure (PCWP)
Serum electrolytes
Routine blood investigations,
Renal Function Test
Liver Function Test,
Complete Blood Count

18. MANAGEMENT
Ventilatory support
Proper oxygenation with intubation
Correction of electrolytes
Relief of pain
Antiarrhythmic drugs
Avoid fluid overload
Prevention of pulmonary oedema
Anticoagulants and aspirin are given
Beta blockers and nitroglycerine are given
Careful judicious use of dopamine and dobutamine are often needed
Treat the cause

19. SEPTIC SHOCK
It is due to bacterial infection which release toxins
leading to shock.

20. May be due to gram positive organisms, gram
negative organisms, fungi, viruses or protozoal origin.
Gram negative septic shock is called as endotoxic
shock and it is caused by organisms like E. Coli,
Klebsiella, pseudomonas and proteus.

21. ETIOLOGY
Peritonitis
Urinary infection
Gastrointestinal fistulas
Biliary infection
Major surgical wounds
Pancreatitis
Diabetic wounds
Crush injuries
Septic shock is typically a vasodilatory shock wherein there is
peripheral vasodilatation causing hypotension which is resistant to
vasopressors.

22. STAGES OF SEPTIC SHOCK
HYPER DYNAMIC SHOCK
(WARM SEPTIC SHOCK)
◦ This stage is reversible stage.
◦ Patient is still having inflammatory response
and so presents with fever, tachycardia and
tachypnoea.
◦ Patient should be treated properly at this
stage.
HYPO DYNAMIC HYPOVOLAEMIC
SEPTIC SHOCK
(COLD SEPTIC SHOCK)
◦ This stage is irreversible stage.
◦ Here inflammatory response is lost.
◦ Patient is in decompensated shock.
◦ This irreversible stage is associated with
multi-organ dysfunction syndrome (MODS),
anuria (kidney failure), respiratory failure
(cyanosis), liver failure (jaundice), cardiac
depression, hypotension, pulmonary oedema,
hypoxia, drowsiness, eventually coma and
followed by death.

23. INVESTIGATIONS
Complete Blood Count (CBC)
Random Blood Sugar (RBS)
Liver Function Test (LFT)
Renal Function Test (RFT)
Viral markers
Pus/ blood/ urine culture and sensitivity
CT Scan
Ultrasound scan to find the source of infection

24. MANAGEMENT
Correction of fluid electrolyte imbalance by crystalloids,
blood transfusion
Third generation antibiotics cephalosporin and
minoglycosides are to be given
Treat the cause, laparotomy for peritonitis, drainage of pus,
resection of gangrenous bowel.
Monitoring of the patient by pulse oximetry, cardiac status,
urine output, arterial blood gas analysis, BP monitoring

25. MANAGEMENT
Ventilator support, ICU management, oxygen
Dobutamine/ dopamine/ noradrenaline to maintain blood pressure and
urine output
Short term high dose steroids injections are to be given to protect the
cells from the effect of endotoxins. It improves cardiac, renal and lung
functions.
Steroids are effective in septic shock

26. NEUROGENIC SHOCK
Occurs due to sudden shocking event or sudden
painful stimuli or injury to spinal cord causing
severe splanchnic vessel vasodilatation

27. ETIOLOGY
It is usually due to spinal
cord injury or some
sudden shocking event or
sudden painful stimulus
which causes dilatation
ofsplanchnic vessels.

28. CLINICAL FEATURES
Hypotension
Bradycardia
Arrhythmias
Decreased cardiac output.

29. TREATMENT
This type can safely be
treated with vasoconstrictor
drugs to bring up the blood
pressure, B.P. control,
oxygen delivery, air way
clearance, fluid therapy,
maintenance of
haemodynamics,
intravenous steroids are to
be given.

30. ENDOCRINE SHOCK
It may present as a combination of hypovolaemic,
cardiogenic and distributive shock.
Causes of endocrine shock include:
i. Hypothyroidism
ii. Hyperthyroidism
iii. Adrenal insufficiency

31. ETIOLOGY
Hypothyroidism causes a shock similar to the one as neurogenic shock. Cardiac
output falls and there is bradycardia. There may also be associated
cardiomyopathy
Hyperthyroidism (thyrotoxicosis) on the other hand causes high output cardiac
failure
Adrenal insufficiency leads to shock due to hypovolaemia and a poor response
to circulating and exogenous catecholamines ( These are hormones
manufactured by the adrenal glands, e.g. adrenaline, dopamine,noradrenaline)
Adrenal insufficiency may be due to a pre-existing Addison's disease or be a
relative insufficiency due to a pathological disease such as systemic sepsis

32. ANAPHYLACTIC SHOCK
•It occurs due to Type I hypersensitivity Reactions.
•Various drugs including antibiotics, anaesthetic drugs, stings,
venoms may be having antigens which may combine with IgE of
mast cells and basophils of host body and release histamines and
large amounts of slow releasing substance of anaphylaxis (SRS-
A).

33. CLINICAL FEATURES
Hypotension
Bronchospasm
Laryngeal oedema
Respiratory distress
Feeble pulse
Rashes all over the body.
MORTALITY RATE IS 10%

34. TREATMENT
Adrenaline 100 microgram i/v Stat
Intravenous fluids
Oxygen
Foot end elevation
Ventilator support in serious cases
Cardiac message may be Required
Defibrillator may be required

36. MILD SHOCK
• Initially there is
• Tachycardia
• Tachypnoea
• A mild reduction in
urine output
• The patient may exhibit
mild anxiety.
• The blood pressure is
maintained.
• The peripheries are cool
and sweaty.
MODERATE
SHOCK
• As the shock progresses
renal compensatory
mechanisms fail, renal
perfusion falls and urine
output dips below
0.5ml/kg/hr.
• There is further
tachycardia, and now the
BP starts to fall.
• Patient becomes drowsy
and slightly confused.
SEVERE SHOCK
• Here there is severe
• Lactic Acidosis
• Anuria
• Tachypnoea with
gasping
• Severe tachycardia
• Profound hypotension
• Unconsciousness .
• From here the patient
may slip to the stage of
coma and ultimately die,
if not taken care of on an
emergency level
SEVERITY OF SHOCK

37. SHOCK INDEX
It is a ratio of pulse to blood pressure.
Normal value is less than one.
In shock the normal value is reversed that is it is more than one.

38. EFFECTS OF SHOCK ON VARIOUS
ORGANS
•Heart
•Lung
•Metabolic
•Cellular changes
•Brain
•Kidneys
•Blood
•Gastro-intestinal tract

39. HEART
◦ Low perfusion
◦ Low venous return
◦ Decreased cardiac output
◦ Hypotension
◦ Tachycardia.
◦ Persistent shock causes hypoxia and
release of myocardial depressants
leading to further cardiac damage

40. LUNG
◦ Interstitial oedema
◦ Decreased gaseous exchange
◦ Pulmonary arteriovenous shunting
◦ Tachypnoea
◦ Acute respiratory distress syndrome
(ARDS)
◦ Pulmonary oedema

41. METABOLIC
◦ Shock leads to hypoxia, which activates anaerobic
metabolism leading to lactic acidosis.
◦ Antidiuretic hormone (ADH) is released which
increases the reabsorption of water from renal
tubules
◦ Other hormones released are Adeno- cortico-trophic-
hormone (ACTH), bradykinin, prostaglandins,
histamines and serotonins to compensate the effects
of shock to increase the perfusion of vital organs like
heart, brain, lungs

42. CELLULAR CHANGES
◦ Cellular changes occur in persistent shock due to release of
lysosomal enzymes which alter the cell membrane permeability
which in turn cause cell death.

43. BRAIN
◦ When the perfusion of the brain decreases, the patient becomes
drowsy.
◦ Brain is the last organ to get under perfused in shock

44. KIDNEYS
◦ Glomerular filtration rate (GFR) decreases and tubular reabsorption of salt
and water increases for compensatory response.
◦ But in severe cases tubular necrosis sets in leading to irreversible damage

45. BLOOD
◦ Alterations in the cellular components of the blood including platelets
leads to disseminated intravascular coagulation (DIC).
◦ It causes bleeding from all the organs

46. GASTRO – INTESTINAL TRACT
◦ Mucosal ischaemia develops
causing bleeding from GIT with
haematemesis and malaena.
◦ It is aggravated by disseminated
intravascular coagulation

47. MULTIPLE ORGAN
DYSFUNCTION SYNDROME
It is the progressive irreversible damage and loss of
functions of all vital organs like liver, lungs kidneys, GIT.

48. ◦ Lungs and liver are commonly involved (70%)
◦ Next organs to be involved are kidneys, GIT.
◦ Order of involvement of organs in Multiple Organ Dysfunction
Syndrome is
LUNGS > RIGHT VENTRICULAR FAILURE > LIVER > KIDNEY
It occurs in critically ill patients after severe trauma, burns, bleeding,
sepsis, pancreatitis etc.
It is more common in elderly, diabetics, smokers, alcoholics, cirrhosis,
malnutrition, uraemia cases, immunosuppressed patients, patients
taking steroids and cytotoxic drugs

49. FEATURES RELATED TO
MULTIPLE ORGAN DYSFUNCTION
SYNDROME
 TypicalOliguria
 Jaundice
 Hypotension
 Drowsiness
 Respiratory distress are common
findings on clinical examination
 Platelets micro aggregation
 Acute pulmonary hypertension
(APH)
Circulatory failure
Acute respiratory distress syndrome
(ARDS)
Disseminated intravascular
coagulation
Impaired defense mechanism are the
pathological features
Respiratory, renal, hepatic,
Circulatory, coagulative and cardiac
failure occurs as end stage of MODS

50. MANAGEMENT OF
MULTIPLE ORGAN
DYSFUNCTION SYNDROME

51. Critical care in ICU
with ventilator
support
Haemodialysis
Intravenous
infusions including
blood transfusion
Hyperbaric oxygen
to be administered
Third stage
cephalosporins
(broad spectrum
antibiotics) are
administered
Nutrition in the
form of TPN (trans
parenteral
nutrition) or enteral
nutrition
TREATMENT OF THE CAUSE IF POSSIBLE
MODS stage has got high mortality.
(Dobutamine raises cardiac output)
(Dopamine is preferred in hypotension cases)