Approach to hypovolemic and septic shock
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Transcript of Approach to hypovolemic and septic shock
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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