APPROACH TO HYPOVOLEMIC AND SEPTIC SHOCK

Prepared by: Dr. Ahmed M. Bahamid pediatric resident at Alsabeen hospital

April 13, 2023

OBJECTIVES

Definition of shock Pathophysiology, common types and

etiologies of shock Clinical manifestations and diagnosis Management of child with septic and

Hypovolemic shock

DEFINITION

Shock is an acute syndrome characterized by the body’s inability to deliver adequate oxygen to meet the metabolic demands of vital organs and tissues.

EPIDEMIOLOGY

Shock occurs in 2% of all hospitalized patients in USA.

Death usually occur due to complications rather than during hypotensive phase

The presence of MODS in patients with shock substantially increases the probability of death

Mortality in septic shock as low as 3% in previously healthy children & 6-9% in children with chronic illness

Early effects of O2 deprivation on the cell are REVERSIBLE

Early intervention reduces mortality

Often masked in pediatrics . Why?

PATHOPHYSIOLOGY

An initial insult triggers shock, leading to inadequate O2 delivery to organs and tissues

Compensatory mechanisms attempts to maintain BP

COMPENSATORY MECHANISMS

Increase HR, stroke volume, & vascular smooth muscle tone. Regulated through sympathetic NS & neurohormonal responses.

Increased RR with greater CO2 elimination is a compensatory response to the metabolic acidosis & increased CO2 production from poor tissue perfusion

COMPENSATORY MECHANISMS

Renal excretion of H ions & retention of bicarbonate also increase in an effort to maintain normal body pH.

Maintenance of intravascular volume is facilitated via sodium regulation through the renin-angiotensin-aldosterone & atrial natriuretic factor axes, cortisol & catecholamine synthesis & release, and ADH secretion.

Despite these compensatory mechanisms, the underlying shock and host response lead to vascular endothelial cell injury and significant leakage of intravascular fluids into interstitial extracellular space.

Initial insult

Triggers shock

Decreased perfusion

Compensatory mechanisms

Compensated shock

Decompensated shock

Tissue damage

Multisystem organ failure

Death

In adequate O2 at tissue level

Anaerobic metabolism with resultant progressive LACTIC

ACIDOSIS

Inadequate

perfusion

persist

Adverse VASCULAR, INFLAMMATORY, METABOLIC, CELLULAR, ENDOCRINE, AND SYSTEMIC responses

Physiological instability

STAGES OF SHOCK

Pathophysiology of shock passes into 3 progressive stages; (INTERVENE EARLY)

1)- compensated shock

2)- decompensated shock

3)- irreversible sock

Why is it important to identify the

stage of shock?

COMPENSATED SHOCK

Compensatory mechanisms attempts to maintain BP

NORMAL BLOOD PRESSURE Unexplained tachycardia Mild tachypnea Delayed capillary refill Orthostatic changes in pressure or

pulse irritability

DECOMPENSATED SHOCK

It is a state of inadequate end-organ perfusion

Compensatory mechanisms fails and HYPOTENSION occurs.

Increased tachycardia, increased tachypnea

Altered mental state, low urine output, Poor peripheral pulses. Capillary refill markedly delayed Cool extremities

IRREVERSIBLE SHOCK

It occurs as a consequence of decompensated shock not managed properly and at right time.

Permanent cellular damage & MODS. Recovery does not occur even with

adequate restoration of circulatory volume

Death occurs due to refractory acidosis, myocardial and brain ischemia.

Pathophysiology of shock

Extracorporeal fluid loss

Hypovolemic shock may be due to direct blood loss through hemorrhage or abnormal loss of body fluids (diarrhea, vomiting, burns, diabetes mellitus or insipidus, nephrosis)

Lowering plasma oncotic pressure

Hypovolemic shock may also result from hypoproteinemia (liver injury, or as a progressive complication of increased capillary permeability)

Abnormal vasodilation

Distributive shock (neurogenic, anaphylaxis, or septic shock) occur when there is loss of vascular tone- venous, arterial or both (sympathetic blockade, local substance affecting permeability, acidosis, drug effects, spinal cord transection)

Increased vascular permeability

Sepsis may change vascular permeability in the absence of any change in capillary hydrostatic pressure (endotoxins from sepsis, and excess histamine release in anaphylaxis)

Cardiac dysfunction

Peripheral hypoprfusion may result from any condition that affects the heart’s ability to pump blood efficiently (ischemia, acidosis, drugs, constrictive pericarditis, sepsis)

In septic shock it is important to distinguish between the inciting infection and the host inflammatory response.

Normally host immunity prevents the development of sepsis via activation of the reticular endothelial systems.

This host immune response produces an inflammatory cascade of toxic mediators, including hormones, cytokines, and enzymes

If this inflammatory cascade is uncontrolled, derangement of the microcirculatory system leads to subsequent organ and cellular dysfunction

Sepsis or tissue hypoxia with lactic acidosis

↓ ATP, ↑ H+, ↑ lactate In vascular smooth

muscle

↑nitric oxide

synthase

↑ vasopressinsecretion

↓ vasopressin

stores

↓ plasma vasopressin

Vasodilatation

Open K ATP

↑nitric oxide

Open K Ca

↓ cytoplasmic Ca 2+

↑ cGMP

↓ phosphorylate

d myosin

SYSTEMIC INFLAMMATORY RESPONSE SYNDROME

SIRS is an inflammatory cascade that is initiated by the host response to an infectious or noninfectious trigger.

This inflammatory cascade is triggered when the host defense system does not adequately recognize and/or clear the triggering event

The inflammatory cascade initiated by shock can lead to hypovolemia, cardiac & vascular failure, ARDS, insulin resistance, decreased CYP450 activity, coagulopathy,..etc

Ait‐Oufella H, et al. Intensive Care Med 2010;26:1286‐1298. Rivers E, et al. NEJM 2001;345:1368‐1377.

SIRSEndothelial activationDisruption of:CoagulationVascular permeabilityVascular tone

Global tissue hypoxiaMicrocirculatory failurePrecipitated by:Cytokines[Over]production of nitricoxideResults in:Loss of vasomotor controlUnder‐perfusion of tissuesHypotension

Organ dysfunction

HeartLungsBrainKidneysLiver

TNF & other mediators increase vascular permeability, causing diffuse capillary leak, decreased vascular tone, and an imbalance between perfusion and metabolic demands of tissues

TNF & IL-1 stimulates the release of pro-inflammatory and anti-inflammatory mediators causing fever and vasodilation

Arachidonic acid metabolites lead to the development of fever, tachypnea, ventilation-perfusion abnormalities, and lactic acidosis.

Nitric oxide released from the endothelium or inflammatory cells, is a major contributor to hypotension.

Myocardial depression is caused by myocardium-depressant factors, TNF, and some interleukins through direct myocardial injury, depleted catecholamines, increased -endorphin, and production of myocardial nitric oxide

The inflammatory cascade is initiated by toxins or superantigens via macrophage binding or lymphocyte activation.

The vascular endothelium is both a target of tissue injury and a source of mediators that may cause further injury.

The balance between these mediator groups for an individual patient contributes to the progression of disease and affects the chance for survival.

Focus of infection

Superantigens or toxins

Activated inflammatory

cells

Activation of host defense

Activ. Of complement

system

Activ. Of coagulation

system

Endogenous mediator release

Pro-inflammatory cytokinesAnti-inflammatory cytokines

Platelet activating factorArachidonic acid

metabolitesMyocardial depressant

substanceEndogenous opiates

Activated endothelium

increased expression endothelial derived adhesion

moleculesDecreased thrombomodulin

Increased plasminogen activator inhibitor

Thrombosis & antifibrinolysis

Hypovolemia, cardiac & vascular failure, capillary leak/endothelial damage, ARDS, DIC, decreased

steroid synthesis

Shock

MODS

Death

INFLAMMATORY MEDIATORS

Pro-inflammatory mediators

Anti-inflammatory mediators

Tumor necrosis factor (TNF)Interleukin-1Interleukin-6Interleukin-8Interleukin-gammaHMGB-1 (high mobility group box chromosomal protein 1)

Interleukin-4Interleukin-10Soluble receptor and receptor antagonists

CLINICAL MANIFESTATIONS

Categorization is important, but there may be significant overlap among these groups, especially in septic shock.

The clinical presentation of shock depends in part on the underlying etiology.

If unrecognized and untreated all forms of shock progresses ultimately to irreversible shock and death.

Shock may initially manifest as only tachycardia or tachypnea.

Progression leads to; Decreased urine output Poor peripheral perfusion Respiratory distress or failure Alteration of mental status Low blood pressure

Because of the compensatory mechanisms hypotension is often a late finding and is not a criterion for the diagnosis of shock

Tachycardia with or without tachypnea, may be the first or only sign of early compensated shock

Hypotension reflects an advanced state of decompensated shock and is associated with increased mortality.

SIGNS OF DECREASED PERFUSION Organ

dysfunction

↓ Perfusion ↓↓ Perfusion ↓↓↓ Perfusion

CNS __ Restless, apathetic, anxious

Agitated/confused, coma

Respiration

__ ↑ Ventilation ↑↑ Ventilation

Metabolism

__ Compensated metabolic acidemia

Uncompensated metabolic acidemia

Gut __ ↑ Motility Ileus

Kidney Decreased urine volume

Oliguria< 0.5 mL/kg/hr

Oliguria/anuria

Increased specific gravity

Skin Delayed capillary refill

Cold extremities Mottled, cyanotic, cold extremities

CVS Increase heart rate 2* increase HR 2* increase HR

Decreased P. pulses

Decreased BP, only central pulses

CRITERIA FOR ORGAN DYSFUNCTIONOrgan system

Criteria for dysfunction

Cardiovascular

Despite administration of isotonic IV fluid bolus ≥ 60 mL/kg in 1 hour: decrease in BP (hypotension) < 5th percentile for age or systolic BP < 2 SD below normal for ageORNeed for vasoactive drug to maintain BP in normal range (dopamine> 5 micro/kg/min or dobutamine, epinephrine, or norepinephrine at any dose) ORTow of the following:Unexplained metabolic acidosis: base deficit > 5 mEq/LIncreased arterial lactate: > 2x upper limit of normalOliguria: urine output < 0.5 mL/kg/hrProlonged capillary refill: > 5 secondsCore to peripheral temperature gap > 3C

CRITERIA FOR ORGAN DYSFUNCTIONOrgan system

Criteria for dysfunction

Respiratory

PaO2/Fio2 ratio < 300 in the absence of cyanotic heart disease or pre-existing lung diseaseORPaCO2 > 65 torr or 20 mm Hg over baseline PaCO2ORProven need for >50% FiO2 to maintain saturation ≥ 92%ORNeed for non-elective invasive or non-invasive mechanical ventilation

Neurologic

GCS score ≤ 11ORAcute change in mental status with a decrease in GCS score ≥ 3 points from abnormal baseline

CRITERIA FOR ORGAN DYSFUNCTION

Organ system

Criteria for dysfunction

Hematologic

Platelet count < 80,000/mm³ or a decline of 50% in the platelet count from the highest value recorded over the last 3 days (for the patient with chronic hematologic or oncologic disorders)ORINR > 2

Renal Serum creatinine ≥ 2x upper limit of normal for age or 2-fold increase in baseline creatinine value

Hepatic Total bilirubin ≥ 4mg/dL (not applicable for newborn)Alanine transaminase level 2x upper limit of normal for age

TYPES OF SHOCK

SHOCK

Hypovolemic

Cardiogenic

Distributive

Obstructive

Septic

WHY IS IT IMPORTANT TO IDENTIFY THE TYPE OF SHOCK?

Because successful management often depends on correct interpretation of the classification of shock, and often, its specific etiology. For example, the interventions for obstructive or Cardiogenic shock will be different from the interventions for distributive shock (which will also change depending on whether the etiology is anaphylaxis or sepsis).

HYPOVOLEMIC SHOCK

Most common cause of shock in children worldwide

Decreased preload due to internal or external losses

Water /electrolyte loss (diarrhea & vomiting)

Blood loss (hemorrhage)

Plasma loss (burns & nephrotic syndrome)

HYPOVOLEMIC SHOCK

Tachycardia and an increase in systemic vascular resistance are the initial compensatory response to maintain cardiac output and blood pressure

Manifests initially as orthostatic hypotension

Associated with dry mucous membranes, dry axillae, poor skin turgor, and decreased urine output.

HYPOVOLEMIC SHOCK

Depending on the degree of the dehydration, the patient with hypovolemic shock may present with either normal or slightly cool distal extremities, and peripheral or central (femoral) pulses may be normal, decreased, or absent.

CARDIOGENIC SHOCK Cardiac pump failure 2ndry to poor

myocardial function

CHD Cardiomyopathies ( infectious or

acquired, dilated or restrictive) Ischemia or arrhythmias

Myocardial contractility affected leading to systolic and/or diastolic dysfunction

CARDIOGENIC SHOCK

Because of decreased CO and compensatory peripheral vasoconstriction, the presenting signs of cardiogenic shock are:

Tachypnea Cool extremities Delayed capillary refill Poor peripheral and/or central pulses Declining mental status Decreased urine output

DISTRIBUTIVE SHOCK

Inadequate vasomotor tone, which leads to capillary leak and maldistribution of fluid into the interstitium

Sepsis, hypoxia, poisonings, anaphylaxis, spinal cord injury, or mitochondrial dysfunction.

↓ in SVR accompanied with maldistribution of blood flow from vital organs and a compensatory increase in CO

This process leads to decrease in preload and afterload

DISTRIBUTIVE SHOCK

Distributive shock manifests early as peripheral vasodilation and increased but inadequate cardiac output

OBSTRUCTIVE SHOCK

Caused by a lesions that creates a mechanical barrier that impedes adequate CO

Decreased CO secondary to direct impediment to right or left heart outflow or restriction of all cardiac chambers.

OBSTRUCTIVE SHOCK

Pericardial tamponade, tension pneumothorax, pulmonary embolism, ductus-dependant CHD

Anterior Mediastinal masses. Critical coarctation of the aorta

OBSTRUCTIVE SHOCK

Obstructive shock often manifests as inadequate cardiac output due to a physical restriction of forward blood flow; the acute presentation may quickly progress to cardiac arrest

Regardless of etiology, uncompensated shock, with hypotension, high vascular resistance, decreased cardiac output, respiratory failure, obtundation, and oliguria, occurs late in the progression of the disease.

Additional clinical findings in shock include cutaneous lesions such as petechiae, diffuse erythema, ecchymoses, erythema gangrenosum, and peripheral gangrene.

jaundice can be present either as a sign of infection or as a result of MODS.

SEPTIC SHOCK

Usually involves a more complex interaction of distributive, Hypovolemic, and Cardiogenic shock

Bacterial Viral Fungal (immunocompromised

patients are at increased risk)

SEPTIC SHOCK

Cardiogenic

Distributive Hypovolemi

c

Sepsis is defined as SIRS resulting from a suspected or proven infectious etiology.

Severe sepsis (the presence of sepsis combined with organ dysfunction.

Septic shock (severe sepsis plus the persistence of hypoperfusion or hypotension despite adequate fluid resuscitation or a requirement for vasoactive agents), MODS, and possibly death.

THE PROGRESSION OF SEPSIS

SIRSFrom

infectionSepsis

Severe sepsis

Septic shock MODS

Death

Outcomes improve with early recognition and treatment

SEPTIC SHOCK

The initial sign and symptoms are; Alteration in temperature regulation

(hypo or hyperthermia) Tachycardia and tachypnea In early stages (hyperdynamic phase or

warm shock) the cardiac output increases in an attempt to maintain adequate O2 delivery and meet the metabolic demands

SEPTIC SHOCK

As septic shock progresses, cardiac output falls in response to the effects of numerous inflammatory mediators, leading to a compensatory elevation in SVR and the development of cold shock

HEMODYNAMIC VARIABLES IN DIFFERENT SHOCK STATES

Type of shock

CO SVR MAP CWP CVP

HYPOVOLEMIC

↓ ↑ ↔ OR ↓ ↓↓↓ ↓↓↓

CARDIOGENIC:

SYSTOLIC ↓↓ ↑↑↑ ↔ OR ↓ ↑↑ ↑↑

DIASTOLIC ↔ ↑↑ ↔ ↑↑ ↑

OBSTRUCTIVE

↓ ↑ ↔ OR ↓ ↑↑ Ω ↑↑ Ω

DISTRIBUTIVE

↑↑ ↓↓↓ ↔ OR ↓ ↔ OR ↓ ↔ OR ↓

SEPTIC:

EARLY ↑↑↑ ↓↓↓ ↔ OR ↓ ‡ ↓ ↓

LATE ↓↓ ↓↓ ↓↓ ↑ ↑ or ↔

DIAGNOSIS

Shock is diagnosed clinically on the basis of a thorough history and physical exam.

DIFFERENTIAL DIAGNOSIS OF THE CHILD PRESENTING WITH SHOCK

Bleeding shock —History of trauma ,Bleeding site

Dengue shock syndrome —Known dengue outbreak or season, History of high fever ,Purpura

Cardiac shock —History of heart disease , congested neck veins and liver

Septic shock —History of febrile illness ,Very ill child Known outbreak of meningococcal infection

Shock associated with severe dehydration —History of profuse diarrhea ,Known cholera outbreak

CHILD WITH SHOCK

TESTING SKIN PINCH FOR ASSESSING DEHYDRATION

LABORATORY FINDINGS

Thrombocytopenia & anemia Prolonged PT & PTT Reduced fibrinogen level Elevation of fibrin split products Elevated neutrophil count and

immature forms, vacuolation of neutrophils, toxic granulations, and Döhle bodies can be seen with infection

Neutropenia & leukopenia are ominous sign of overwhelming sepsis.

LABORATORY FINDINGS

Glucose dysregulation (hyper or hypoglycemia) is a common stress response

Electrolyte abnormalities are hypocalcemia, hypoalbuminemia, and metabolic acidosis.

Renal and/or hepatic function may be abnormal

Patients with ARDS or pneumonia have impairment of oxygenation (decreased PaO2) as well as ventilation (increased PaCO2) in the later stage of lung injury.

LABORATORY FINDINGS

The hallmark of uncompensated shock is an imbalance between O2 delivery and O2 consumption.

This state manifests clinically by increased lactic acid production (high anion gap, metabolic acidosis) due to anaerobic metabolism and a low mixed venous oxygen saturation

LABORATORY FINDINGS

Serum lactate measurement along with mixed venous oxygen saturation may be used as a marker for the adequacy of oxygen delivery and the effectiveness of therapeutic interventions.

TREATMENT

INITIAL MANAGEMENT

Early recognition and prompt intervention are extremely important in the management of all forms of shock.

INITIAL MANAGEMENT

Regardless of the cause: ABC’s First assess airway patency, ventilation, then

circulatory system Respiratory Performance

Respiratory rate and pattern, work of breathing, oxygenation (color), level of alertness

Circulation Heart rate, BP, perfusion, and pulses, liver size CVP monitoring may be helpful

INITIAL MANAGEMENT

Airway management Always provide supplemental oxygen Endotracheal intubation and controlled

ventilation is suggested if respiratory failure or airway compromise is likely

elective is safer and less difficult decrease negative intrathoracic pressure improved oxygenation and O2 delivery and

decreased O2 consumption

INITIAL MANAGEMENT

Neonates and infants in particular may have profound glucose dysregulation in association with shock

Glucose levels should be checked routinely and treated appropriately, especially early in the course of the illness.

INITIAL MANAGEMENT

Given the predominance of sepsis and hypovolemia as the most common causes of shock in the pediatric population, most therapeutic regimens are based on guidelines established in these settings.

INITIAL MANAGEMENT

Immediately after establishment of IV or IO access, aggressive, early goal-directed therapy (EGDT) should be initiated unless there significant concerns for cardiogenic shock as an underlying pathophysiology.

INITIAL MANAGEMENT

Rapid IV administration of 20 mL/kg isotonic saline or, less often colloid should be initiated in an attempt to reverse the shock state

Bolus should be repeated quickly up to 60-80 mL/kg.

Rapid fluid resuscitation using 60-80 mL/kg or more is associated with improved survival without an increased incidence of pulmonary edema.

INITIAL MANAGEMENT

Fluid resuscitation in increments of 20 mL/kg should be titrated to normalize HR, urine output (to 1 mL/kg/hr), capillary refill time(<2 seconds), and mental status.

Normalization of BP alone is not a reliable endpoint for assessing the effectiveness of resuscitation.

INITIAL MANAGEMENT

Although the type of fluid (crystalloid vs colloid) is an are of debate, fluid resuscitation in the first hour is unquestionably essential to survival in septic shock, regardless of the fluid type administered.

If shock remains refractory following 60-80 mL/kg resuscitation, inotrope therapy should be instituted while additional fluid are administred

INITIAL MANAGEMENT

Inotropic and vasoactive drugs are not a substitute for fluid, however... Can have various combinations of

hypovolemic and septic and cardiogenic shock

May need to treat poor vascular tone and/or poor cardiac function

CARDIOVASCULAR DRUG TREATMENT OF SHOCK

Drug Effects Dosing range comments

Dopamine ↑ cardiac contractility

3-20 microg/kg/min

↑ risk of arrhythmias with high doses

Significant peripheral vasoconstriction at > 10 micro/kg/min

Epinephrine

↑ HR, ↑ cardiac contractility

0.05-3 mic/kg/min

May ↓ renal perfusion at high dosesPotent

vasoconstrictor ↑ myocardial O2 consumption

Risk of arrhythmias at high doses

Dobutamine

↑ cardiac contractility

1-10 micro/kg/min

___

Peripheral vasodilator

Norepinephrine

Potent vasoconstriction

0.05-1.5 micro/kg/min

↑ BP 2ndry to ↑ SVR

No significant effect on cardiac contractility

↑ left ventricular afterload

Phenylephrine

Potent vasoconstriction

0.5-2 micro/kg/min

Cause sudden hypertension

↑ O2 consumption

VASODILATORS/AFTERLOAD REDUCERS

Drug Effects Dosing range comments

Nitroprosside

Vasodilator (mainly arterial)

0.5-4 mic/kg/min

Rapid effectRisk of cyanide toxicity with use >96hr

Nitroglycerine

Vasodilator (mainly venous)

1-20 mic/kg/min

Rapid effectRisk of ↑ ICP

Prostaglandin E1

vasodilator 0.01-0.2 mic/kg/min

Can lead to hypotensionRisk of apnea

Maintain an open ductus arteriosus

Milrinone Increased cardiac contractility

Load 50 mic/kg over 15 min

Phosphodiestrase inhibitor – slow cyclic adenosine monophosphate breakdown

Improves cardiac diastolic function

0.5-1 mic/kg/min

Peripheral vasodilation

GOAL-DIRECTED THERAPY OF ORGAN DYSFUNCTION IN SHOCK

System Disorder Goals therapies

Respiratory

ARDS Prevent/treat; hypoxia & respiratory acidosis

Oxygen

Respiratory muscle fatigue

Prevent barotrauma

Early endotracheal intubation & mechanical ventilation

Central apnea Decrease work of breathing

PEEPPermissive hypercapniaHigh-frequency ventilationECMO

GOAL-DIRECTED THERAPY OF ORGAN DYSFUNCTION IN SHOCK

System

Disorder Goal Therapies

Renal

Prerenal failure

Renal failure

Prevent/treat; hypovolemia, hypervolemia, hyperkalemia, metabolic acidosis, hypernatremia/hyponatremia, & hypertension.

Monitor serum electrolytes

Judicious fluid resuscitationLow-dose dopamine

Establishment of normal urine output & BP for age

Furosemide (Lasix)

Dialysis, ultrfiltration, hemofiltration

GOAL-DIRECTED THERAPY OF ORGAN DYSFUNCTION IN SHOCK

System Disorder Goal Therapies

Hematologic

Coagulopathy (DIC)

Prevent/treat; bleeding Vitamin K

Fresh frozen plasma

Platelets

Thrombosis Prevent/treat; abnormal clotting

Heparinization

Activated protein C

GOAL-DIRECTED THERAPY OF ORGAN DYSFUNCTION IN SHOCK

System

Disorder Goal Therapies

GIT Stress ulcer Prevent/treat; gastric bleedingAvoid aspiration, abdominal distension

Histamine H2 receptor-blocking agents or proton pump inhibitors

Nasogastric tube

Ileus Bacterial translocation

Avoid mucosal atrophy Early enteral feedings

GOAL-DIRECTED THERAPY OF ORGAN DYSFUNCTION IN SHOCK

System Disorder Goal Therapies

Endocrine

Adrenal insufficiency, primary or secondary to chronic steroid therapy

Prevent/treat; adrenal crisis

Stress-dose steroid in patients previously given steroids

Physiologic dose for presumed primary insufficiency in sepsis

Metabolic

Metabolic acidosis

Correct etiology

Normalize pH

Treatment of hypovolemia (fluids) & poor cardiac function (fluids, inotropic agents)Improvement of renal acid excretionLow-dose (0.5-2 mEq/kg) sodium bicarbonate if the patient is not showing response, pH < 7.1, and ventilation (CO2 elimination) is adequate.

SEPTIC SHOCK

Early administration of broad spectrum antimicrobial agents is associated with a reduction in mortality.

Neonates should be treated with ampicillin plus cefotaxime and/or gentamicin. Acyclovir should be added if herpes simplex virus is suspected clinically.

SEPTIC SHOCK

In infants and children Community acquired N. meningitides

can be treated with 3rd generation cephalosporin (Ceftriaxone or cefotaxime) or high dose penicillin.

H. influenzae can be treated with ceftrixone or cefotaxime

The presence of resistant S. pneumoniae often requires the addition of vancomycin

SEPTIC SHOCK

Suspicious of community or hospital acquired MRSA infection warrants the coverage with vancomycin.

If intra-abdominal process is suspected, anaerobic coverage should be included with an agents such as Metronidazole, Clindamycin, or piperacillin-tazobactam.

SEPTIC SHOCK

Nosocomial sepsis should generally be treated at least 3rd or 4th generation cephalosporin or piperacillin-tazobactam. An aminoglycoside should be added as the clinical situation warrants.

Vancomycin should be added to the regimen if the patient has an indwelling medical device, gram positive cocci are isolated from the blood, or MRSA is suspected or as empiric coverage for S. pneumoniae.

SEPTIC SHOCK

Empirical coverage for fungal infections should be considered for selected immunocompromised patients.

These broad, generalized recommendations must be tailored to the individual clinical scenario and to the local resistance pattern of the community and/or hospital

HYPOVOLEMIC SHOCK

Mainstay of therapy is fluid Goals

Restore intravascular volume Correct metabolic acidosis Treat the cause

Degree of dehydration often underestimated Reassess perfusion, urine output,

vital signs... Isotonic crystalloid is always a good choice

Regardless of the etiology of shock, metabolic status should be meticulously maintained.

Electrolytes should be monitored closely and corrected as needed.

Hypoglycemia is common and should be promptly treated.

Hypocalcemia which may contribute to myocardial dysfunction, should be treated.

STEROIDS

Hydrocortisone replacement may be beneficial in pediatric shock.

Up t0 50% of critically ill patient may have absolute or relative adrenal insufficiency.

Patients at increased risk for adrenal insufficiency include those with congenital adrenal hyperplasia, abnormalities of hypothalamic-pituitary axes, recent therapy with corticosteroids, and should receive stress doses of hydrocortisone.

STEROIDS

Steroids may also be considered in patients with shock that is unresponsive to fluid resuscitation and catecholamines.

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