A postgraduate seminar on

shock
Presented by Boma George
Dept. of Pediatrics
FMC Yenagoa
 Outline
• Introduction
• Epidemiology
• Types
• Pathophysiology
• Clinical presentation
• Investigation
• Management
• conclusion
 Introduction

Shock is an emergency clinical condition;

• Involves:
• Inadequate organ & tissue perfusion due
to circulatory failure.
• Profound haemodynamic & metabolic
disturbances
 Introduction contd
• Defined as the inability of the body to
deliver adequate oxygen to meet its
metabolic needs due to impaired tissue
perfusion
• A complex clinical syndrome in which the
cardiovascular system fails in its primary
function of substrate delivery and
metabolite removal, resulting in anaerobic
metabolism and tissue acidosis
 Introduction contd
• Circulatory function is dependent on
– Blood volume
– Vascular tone, and
– Cardiac function
• Shock states may result from
abnormalities in one or more of these
factors
 Epidemiology
• Shock occurs in approximately 2% of all
hospitalized infants, children, and adults in the
USA (≈400,000 cases/year), and the mortality rate
varies according to the clinical circumstances

• Dehydration and hypovolemic shock alone result

in 6-20 million deaths annually in infants and
children worldwide

• A study done in Addis Ababa, showed that the

overall prevalence of septic shock was 26.5 per
100 ICU admissions
 Epidemiology contd.
• Out of the 670 admissions over a one year
period in FMC Yenagoa ( February 2020 to
January 2021)

• There were 17 (2.5%) cases of septic shock

• Six (35%) were cases of hypovolemic shock

and 11 (65%) cases of hypovolemic shock
• Case fatality rate was 23.5%
 Classification
• Hypovolemic
• Distributive
• Cardiogenic
• Obstructive
• Dissociative

Each type is characterized by one primary

physiologic derangement.

An exception to this is septic shock which has

components of hypovolemic, distributive and
cardiogenic shocks
 Hypovolemic shock
• Absolute reduction in intravascular volume
• Most common type of shock in children in
developing countries
• Causes
– Vomiting and diarrhoea
– Haemorrhage
– Increased insensible losses (burns and fever)
– Diabetes insipidus
– Third space losses (ascites)
10
 Septic Shock
• Encompasses multiple forms of shock:
– Hypovolemic: third spacing of fluids into the
extracellular, interstitial space
– Distributive: early shock with decreased
afterload
– Cardiogenic: depression of myocardial function
by endotoxins

• Causes include infection with viral and

bacterial pathogens, and fungal pathogens
especially in immunocompromised patients
 Distributive Shock
• Abnormalities of vasomotor tone with
consequent increase in venous (and
arterial) capacitance
• Causes include
– Anaphylaxis
– Spinal cord or brainstem injury
– Drugs
– Sepsis
 Cardiogenic Shock
• Cardiogenic shock results from pump failure,
manifested physiologically as decreased
systolic function and depressed cardiac output
• Causes;
– Cardiomyopathies(Familial, Infectious, Infiltrative,
Idiopathic)
– Arrhythmias(Drug intoxications, Metabolic
Acidosis, Hypothermia, Electrolyte derangements)
– Obstructive lesions(Coarctation of the Aorta,
Hypoplastic left ventricle Syndrome, Cardiac
Tamponade, Tension Pneumothorax, Massive
Pulmonary Embolism)
 Dissociative

• This results from markedly inadequate

oxygen delivery or severely impaired oxygen
releasing capacity
• Its causes include:
– Severe anaemia
– Methhaemoglobinaemia
– Carbon Monooxide Poisoning
– Cyanide Intoxication

15
 PATHOPHYSIOLOGY
• Irrespective of aetiology, the pathophysiology
of shock stems from a failure of cellular
aerobic metabolism precipitated by
hypoperfusion and hypoxia
• An index event leads to reduced tissue
perfusion
• Compensatory mechanisms are activated
• In time these mechanisms become
overwhelmed if the constraint persists
• Decompensation develops leading to
hypotension and multiorgan dysfunction
which may ultimately culminate in death
16
 PATHOPHYSIOLOGY
• Shock is a progressive disorder that can be
divided into 3 stages
COMPENSATED SHOCK
• Perfusion to vital organs is maintained via
Sympathetic reflexes and hormonal
mechanisms(Renin-Angiotensin-
Aldosterone System, Vasopressin)
• Derangement of vital signs is minimal
• Exhaustion or inadequacy of this phase
leads to decompensated shock
17
 PATHOPHYSIOLOGY
DECOMPENSATED SHOCK
•As compensatory mechanisms fail, delivery of
oxygen and nutrients to tissues become inadequate

•Hypoxia sets in, aerobic respiration fails and

anaerobic metabolism becomes the main source
of energy generation

•This leads to failure of oxidative phosphorylation,

excessive production of lactic acid, metabolic
acidosis and failure of Na-KATPase
+
+
•Ultimately, intracellular oedema develops,
intracellular contents leak into the extracellular
space and cell death ensues 18
 PATHOPHYSIOLOGY
DECOMPENSATED SHOCK
• There is also an associated release of chemical
mediators, enzymes, and other substances
including histamine, cytokines, nitric oxide,
platelet aggregating factor

• Acidosis reduces myocardial contractility and

impairs its response to catecholamines

• Other mediators contribute to disruption of the

integrity of the capillary endothelium, plasma
protein leaks, loss of oncotic pressure,
extravasation of plasma into the extravascular
space, and stasis in small vessels due to
vasodilation 19
 PATHOPHYSIOLOGY
DECOMPENSATED SHOCK
• Stasis of blood in small vessels promote platelet
adhesion and activation of the coagulation
cascade, which may lead to a bleeding tendency
and further volume depletion, worsening the
hypoperfusion

• Patients with decompensated shock present with

prolonged capillary refilling time, cold, clammy
skin, tachycardia, rapid breathing, altered
consciousness, reduced or absent urine output

• If effective, timely intervention is not instituted, it

will progress to irreversible shock 20
 PATHOPHYSIOLOGY
IRREVERSIBLE SHOCK

• Cellular and tissue damage is so severe

that even if hemodynamic disorders are
corrected, survival is not possible

21
 Pathophysiology contd.
Myocardial dysfunction/obstruction
Sepsis
Vascular tone abnormality
Hpovolaemia
Inadequate tissue perfusion

Metabolic acidosis
Cell/tissue hypoxia
Switch from aerobic to anaerobic metabolism

Energy deficit
→
Lactic acid accumulation and fall in pH

Loss of function Na/K-ATPase with influx Na & water & efflux K

Cell swells, ruptures and dies

24
 Evaluation
• History
– Fever
– Fast/Difficult breathing
– Cough
– Bluish lips, palms, soles
– Wheeze
– Poor feeding/Difficulty with feeding
– Vomiting
– Diarrhoea
– Bleeding
 Evaluation contd
– Body/Abdominal swelling
– Generalized body weakness
– Trauma
– Convulsions
– Loss of consciousness
– Reduced/increased urine output
– Intoxications
– Envenomation
 Evaluation contd
• Past Medical history
– Congenital heart disease
– Recent heart surgery
– Allergies
– Medications/Medical conditions

• Other aspects of history

 Physical examination
General
– Acutely ill
– Agitated/lethargic
– Sunken fontanel
– Sunken eyes
– Dyspnoeic
– Pale
– Icteric
– Cyanosed
– Febrile
28
 Physical examination
General contd
– Dry buccal mucosa
– Cold, clammy skin
– Poor skin turgor
– Capillary refill >2 seconds
– Oedema

CNS
– Confused
– Stuporous
– Comatose

29
 Physical examination
Respiratory system
– Dyspnoea
– Tachypnoea/Hyperpnoea
– Chest wall; Symmetric/asymmetric
– Chest Movement: Equal/unequal
– Trachea: Central/deviated
– Percussion notes: Normal/hyperresonant/dull/
stony dull
– Distant/reduced breath sounds
– Crepitations
30
 Physical examination
Cardiovascular system
– Tachycardia
– Weak/absent peripheral pulses
– Hypotension
– Narrow/wide pulse pressure
– Raised jugular venous pressure
– Hyperactive precordium
– Displaced apex beat
– Distant heart sounds
– Murmurs
– Gallop rhythm

31
 Physical examination
Digestive system
– Abdomen: Distended
– Hepatomegaly
– Ascites
– Bowel sounds: Normal/decreased/increased
Intergumentary system
– Petechiae, ecchymosis, purpura
– Bleeding from mucous membranes

32
 Clinical presentation

Hypovolemic shock
• dry mucous membranes
• reduced skin turgor
• decreased urine output
• Cool-clammy extremities
• ↓↓ or absent peripheral
pulses
 Clinical presentation contd.
Septic shock
• Temperature dysregulation
(hyperthermia or hypothermia)
• tachycardia, and tachypnea
• Petechial haemorrhages
• Other signs of infection
 Clinical presentation contd.
• In the early stages of septic
(hyperdynamic phase or “warm” shock),
the cardiac output increases in an attempt
to maintain adequate oxygen delivery to
the organs and tissues
• As it progresses, cardiac output falls,
leading to a compensatory elevation in
systemic vascular resistance and the
development of “cold” shock
 Signs of decreased perfusion
ORGAN ↓ PERFUSION ↓↓ PERFUSION ↓↓↓ PERFUSION
SYSTE
M
CNS --- Restless, apathetic, Agitated/confused,
anxious stuporous, coma
Resp --- ↑ Ventilation ↑↑ Ventilation
Metabo --- Compensated metabolic Uncompensated
lic acidemia metabolic acidemia
Gut --- ↓ Motility Ileus
Kidney ↓ Urine volume Oliguria (<0.5 mL/kg/hr) Oliguria/anuria
↑ Urinary specific
gravity
Skin Delayed capillary Cool extremities Mottled, cyanotic, cold
refill extremities
CVS ↑ Heart rate ↑↑ Heart rate ↑↑ Heart rate
↓ Peripheral pulses ↓ Blood pressure,
central pulses only
 Investigations
• RBS-treat as appropriate
• EUCr, - metabolic acidosis, ↑Urea and
↑Creatinine
• Serum lactate
• Urinalysis
• Pulse oximetry
• FBC: Hb, WBC, Plt
• Clotting profile: deranged in DIC
• Blood culture
• Chest x-ray: cardiomegaly in CCF
 Investigations contd.
• LFT
• Blood gas analysis
• B-type Natriuretic Peptide (BNP)
• Cardiac Index: CO/BSA – normal 3.3 and
6.0 L/min/m2
• Mixed venous oxygen saturation (SvO2) –
normal 65 – 77%
• Near-infrared spectroscopy (NIRS):
continuous, noninvasive, bed-side
monitoring of tissue oxygenation
 Principles of Management
Shock is an emergency
• ABC of resuscitation
• Fluid Management
• Treat underlying cause
• Supportive management
 Initial resuscitation
• Should commence immediately at diagnosis
• It is essential basic therapy aimed at CAB within the
first hour with intent at:
– Reversing circulatory compromise
– Providing a patent airway
– Determining the adequacy of ventilation
– Giving high-flow oxygen

• Patient should be placed immediately on non-

invasive monitors such as the Pulse Oximeter,
Cardiorespiratory Monitor
• Nurse patient head down
41
 Cardiovascular support
Adequate vascular access
• 2 peripheral intravenous access using the widest
bore cannulae appropriate for age
• Intraosseous access 2-3 cm inferomedial to the
tibial tuberosity or 3-4 cm superior to the medial
epicondyle of the femur, if IV failed

Fluid resuscitation
• The volume of fluid is determined by the clinical
response of the patient
• The volume of fluid must be rapid enough to allow
time for reassessment of the child’s volume and
perfusion status, as well as preparation for
repeated fluid administration, if necessary
42
 Cardiovascular support contd
• The IVFs of choice are the crystalloids -Normal
Saline and Ringer’s Lactate at 20 mL/kg in less
than 5 but up to 15 minutes using the push-pull
method

• As soon as the first bolus has been given,

reassess and immediately administer additional
20mL/kg if signs of poor perfusion persist

• Ultimately the child in shock may receive 60 mL/

kg or more of volume in the first 60 minutes, if
there is severe hypovolaemia or septic shock
43
 Cardiovascular support contd
• Fluid resuscitation in boluses of 20 mL/kg
should be continued until normalization of
– Heart rate (according to age-based heart rates)
– Urine output (to 1 mL/kg/hr)
– Capillary refill time (to <2 sec), and
– Mental status
• Reassess after each bolus of 20ml/kg
• Other fluids that can be used
– Whole blood transfusion
– Albumin and other Colloids infusions
• Albumin and colloids have not
demonstrated any advantage over
crystalloids
 Cardiovascular support contd
• If rales or hepatomegaly develop at any
point during the resuscitation, transition
from fluid administration to inotropic
therapy initiation is indicated

• Transfusion may be required during

resuscitation if a patient with haemorrhage
has received 2-3 boluses of crystalloids

46
 PRECAUTIONS
 Cardiogenic shock
– Judicious fluid boluses of 5-10 mL/kg should be
utilised and balanced with the need for early
inotropic support to prevent fluid overload
 Severe Malnutrition
– 15 mL/kg of Glucose containing fluid over 60
minutes, repeat if response was good, then
commence ORT
 DKA
– 10 mL/kg over 60 minutes

47
 Cardiovascular support contd
 Severe Anaemia

• Children who receive aggressive fluid resuscitation

early have the best chance of surviving severe septic
shock or shock and dehydration

• One large study in African children presenting with

apparent sepsis in resource-limited facilities
demonstrated a worse outcome for children treated
with what would be considered standard fluid
resuscitation

48
 Cardiovascular support contd
INOTROPIC AND VASOACTIVE AGENTS are
indicated in fluid refractory shock
• IV Dopamine 5-20 mcg/kg/min
• IV Epinephrine(Adrenalin) 0.05-1.0 mcg/kg/
min
• IV Dobutamine 2.5-5.0 mcg/kg /min
• IV Milrinone 0.25-1.0 mcg/kg/min
• IV Norepinephrine(Noradrenalin) 0.05-5
mcg/kg/min
• IV Vasopressin
49
 Cardiovascular support contd
• If the shock is refractory to inotropic and
vasoactive agents, further interventions
and investigations should be carried out to
rule out other causes
• This should be done in the PICU

50
 Respiratory support
Assess for airway patency and breathing
• If not patent, clear obstructions or intubate, if
necessary, to maintain patency
• If spontaneous respiration is present, give
high-flow 100% supplemental oxygen via face
mask, nasal prongs or Continuous Positive
Airway Pressure
• Mechanical ventilation is indicated if the
patient is in respiratory failure or if FiO2 is not
adequate to maintain SPO2 more than 92%
• Do ABG 10-15 minutes after respiratory
support has been established
51
 Management contd
• Septic shock: iv broad-spectrum
antibiotics

• Distributive shock: early commemcement

of a vasoconstrictive agents
– Phenylephrine or vasopressin for spinal cord
injury and spinal shock
– Epinephrine for anaphylaxis
 Management contd
• In cardiogenic shock, smaller fluid
boluses (5-10 mL/kg)
• Early commencement of inotropic drugs
(dopamine or epinephrine)
• Also inodilators, such as milrinone
• Agents that increase SVR, such as
norepinephrine and vasopressin, should
be avoided
 Management contd
• In obstructive shock, fluid resuscitation also
given but as a temporizing measure
• The primary insult must be immediately
addressed
– pericardiocentesis for pericardial effusion
– pleurocentesis or chest tube placement for
pneumothorax
– thrombectomy/thrombolysis for pulmonary
embolism
– prostaglandin infusion for ductus-dependent
cardiac lesions
 Management contd
• The use of corticosteroids in shock,
particularly septic shock, is controversial

• However, Steroid may be used in critically

ill patients in shock who may have
absolute or relative adrenal insufficiency
 Management contd
• Such patients include those with
– Waterhouse-Friderichsen syndrome
– congenial adrenal hyperplasia
– abnormalities of the hypothalamic-pituitary axis
– recent therapy with corticosteroids (cases of
asthma, rheumatic diseases, malignancies, and
inflammatory bowel disease)
• Given at stress-dose: 50-100mg/m2/day IV
Hydrocortisone
 Management contd
• Steroids may also be indicated in patients
with shock that are unresponsive to fluid
resuscitation and catecholamine
• Baseline serum cortisol levels should be
checked prior to steroid administration
 Management contd
• Sodium bicarbonate use in the treatment
of shock is controversial
• During shock, acidosis develops, which
impairs myocardial contractility and
optimal function of catecholamine
• However, treatment with bicarbonate may
worsen intracellular acidosis while it
corrects serum acidosis
 Management contd
• This occurs because bicarbonate is an ion
that does not readily traverse
semipermeable cell membranes
• Hence, bicarbonate combines with acid in
serum, resulting in the production of carbon
dioxide and water
• If the increased carbon dioxide is not
removed via ventilation, it readily enters the
cell and drives increasing intracellular
acidosis
 Management contd
• Thus, acidosis that results from shock
should ideally be corrected with increased
perfusion from volume supplementation
and judicious use of cardiotropic
medications together with optimal
ventilation
• However in patients with persistent shock
or ongoing bicarbonate loss (eg, severe
diarrhoea), careful replacement of
bicarbonate may be indicated
 Management contd
• If shock remains refractory despite
maximal therapeutic interventions,
mechanical support with extracorporeal
membrane oxygenation (ECMO) or a
ventricular assist device (VAD) may be
indicated, in an intensive care setting
 Supportive treatment
• Oxygen therapy
• Elevate foot of the bed
• Monitor urine output
• Strict input/output documentation
• Glucose infusion in hypoglycaemia
• May require intubation
• Correct electrolyte derangement(s)-hypo/
hypernatraemia, hypocalcaemia, metabolic
acidosis
 CARDIOVASCULAR DRUG TREATMENT OF
SHOCK
Drug Effect(s) Dosing Comment(s)
Range
Dopa ↑ Cardiac 3-20 µg/ ↑ Risk of arrhythmias at
mine contractility kg/min high doses
Significant
peripheral
vasoconstriction at >
10 µg/kg/min
Epinep ↑ Heart rate and ↑ 0.05-3.0  May ↓ renal perfusion at
hrine cardiac contractility µg/kg/ high doses
Potent min ↑ Myocardial O2
vasoconstrictor consumption
Risk of arrhythmia at
high doses
 CARDIOVASCULAR DRUG TREATMENT OF
SHOCK contd.
Drug Effect(s) Dosing Comment(s)
Range
Norepin Potent 0.05-1.5 µ ↑ Blood pressure
ephrine vasoconstriction g/kg/min secondary to ↑
No significant systemic vascular
effect on cardiac resistance
contractility ↑ Left ventricular
afterload
Phenyle Potent 0.5-2.0 µg Can cause sudden
phrine vasoconstriction /kg/min hypertension
↑ O2 consumption

Dobuta ↑ Cardiac 1-10 µg/ ---

mine contractility kg/min
Peripheral
vasodilator
 Literature review
• A Hospital based longitudinal study done in
Kenyatta National Hospital, Uganda
• Between September to October 2016,
amongst children aged 0 days (≥37 weeks)
to 12 years, showed that the prevalence of
septic shock was 50(15.4%), with a median
age of 4months
• Case fatality rate was highest amongst
infants (82.6%
 Conclusion
• Shock is a well know cause of morbidity
and mortality in children
• Early recognition and prompt intervention
are extremely important for a good
outcome in the management of all forms
of shock
• Refractory shock SHOULD be managed in
intensive care settings
Thank you for
listening
 References
• Turner DA, Cheifetz IM. Shock. In Nelson Textbook of Pediatrics,
19th Edition
• Nadel S, Kissoon N, Ranjit S. Recognition and Initial Management of
Shock. In Roger's Textbook of Pediatric Intensive Care, 4th Edition
• Schwarz AJ, Corden TE. Shock in Pediatrics. http://emedicine.
medscape.com/article/1833578-overview#showall
• Treatment of dehydrated patients. Readings on diarrhoea, student
manual
• Maitland K, Kiguli S, Opoka RO et al. Mortality after Fluid Bolus in
African Children with Severe Infection. http://www.nejm.org/doi/
full/10.1056/NEJMoa1101549#Background=&t=articleBackground
• Carcillo JA, Davis AL, Zaritsky A. Role of early fluid resuscitation in
pediatric septic shock. JAMA. Sep 4 1991;266(9):1242-5

• Postgraduate seminar on shock by Silver Yebaike