General Information
• Shock is observed in 2% of hospitalized patients. The mortality rate varies between 20-50%.
• Multiple organ dysfunction syndrome increases the risk and rate of death (mortality 25% in 1 organ failure, 60% in two organs, and >85% in 3 or more organ failures)
Definition
• Sepsis is defined as an infection-related systemic inflammatory response syndrome.
• There are 5 major types of shock:
hypovolemic, septic, cardiogenic, distributive and obstructive
• The most common types of shock in children are hypovolemic and septic shock.
Definition of SIRS, sepsis, severe sepsis and septic shock
systemic inflammatory response syndrome (SIRS)
At least two of the following criteria (one of which must be abnormal body temperature or white blood cell count)
- Body temperature >38.5 °C or <36 °C (through rectal, oral, bladder or central catheter)
- Tachycardia: mean heart rate >2 SD without external stimuli, chronic drug use, or pain OR unexplained elevation between 0.5 and 4 hours OR <1 age persistent bradycardia lasting longer than 0.5 hours (mean without vagal stimulation, beta-blocker use, or congenital heart disease) heart rate < 10 percentile)
- Respiratory rate > 2 SD for age or need for mechanical ventilation (not due to general anesthesia or neuromuscular disease)
- Leukocytosis or leukopenia (not due to chemotherapy) or >10% immature neutrophils, two of the 4 criteria are present in the diagnosis of SIRS (One of these criteria must be abnormal body temperature or abnormal leukocyte count)
sepsis
Having SIRS with proven or suspected infection
severe sepsis
One of the following with sepsis:
• Cardiovascular organ dysfunction or
• acute respiratory distress syndrome or
• 2 or more organ dysfunction
septic shock
Sepsis and cardiovascular dysfunction
Organ failure criteria
cardiovascular system
Despite administration of 60 ml/kg or more of intravenous isotonic fluid within one hour
• If blood pressure is < 5th percentile (for age) or systolic blood pressure is <2 SD (for age)
OR
• If a vasoactive agent is needed to keep blood pressure within normal limits (dopamine >5 µg/kg min or any dose of dobutamine, epinephrine or norepinephrine needed)
OR
• Any two of the following:
Unexplained metabolic acidosis: Base deficit > 5 mEq/L
Increase in arterial lactate level (more than 2 times the upper limit)
Oliguria: Urine output <0.5 ml/kg/h
Prolongation of capillary refill time: >5 seconds
Rectal - peripheral temperature difference > 3 ° C
The respiratory system
• PaO/FiO2 < 300 without cyanotic heart disease or prior lung disease
OR
• PaCO2 > 65 torr or above 20 mmHg baseline
OR
• Proven need for O2
or
> 50% FiO2 needed to maintain O2 saturation at 92%
OR
• The need for non-elective invasive or non-invasive mechanical ventilation
neurological system
• Glasgow coma score 11
• Acute change in consciousness with more than 3 drop in Glasgow coma score
hematological system
• Platelet count < 80,000/mm 3 or a decrease of more than 50% (based on the highest recorded value in the last 3 days)
• INR > 1.5 or aPTT>60 seconds
renal system
• Serum creatinine 2 times higher than age-appropriate level or 2 times higher than basal creatinine
hepatic system
• Total bilirubin 4 mg/ dl (not used in newborns)
• ALT 2 times higher than the age-appropriate upper limit
Pathophysiology:
• The event that triggers the shock causes insufficient tissue perfusion.
• Compensatory mechanisms in the body are activated and ensure the continuation of the perfusion of vital organs (compensated shock).
• If the patient is not treated during this period, decompensated shock develops, tissue damage occurs, and multiple organ dysfunction develops and the patient dies.
Shock Compensation
• Increase in heart rate
• Increase in stroke volume
• Increase in vascular smooth muscle tone
• Increased respiratory rate (increased CO2 production and metabolic acidosis are compensated)
• Increase in renal hydrogen excretion and bicarbonate reabsorption (pH is brought to normal)
• The provision of intravascular volume is achieved by renin-angiotensin aldosterone, ANF, cortisol and catecholamine synthesis and ADH release.
Pathophysiology of shock
Extracorporeal fluid loss
Hypovolemic shock-may be due to direct blood loss with bleeding or abnormal body fluid loss (diarrhea, vomiting, burns, diabetes insipidus, nephrosis)
Decrease in plasma oncotic pressure
Hypovolemic shock may also develop from hypoproteinemia or be a progressive complication of increased capillary permeability.
abnormal vasodilation
Circulatory shock (neurogenic, anaphylaxis, and septic shock) occurs when intravascular fluid shifts towards the extracellular part due to increased blood flow, blood volume, or hydrostatic pressure in the vascular compartment (sympathetic blockade, local factors affecting permeability, acidosis, drug effect, spinal transection, etc.).
Increased vascular permeability
Sepsis can change capillary permeability without changing capillary hydrostatic pressure (sepsis-related endotoxins, excessive histamine release in anaphylaxis, etc.).
cardiac dysfunction
Peripheral hypoperfusion can develop in any condition that prevents the heart from pumping effectively (ischemia, acidosis, drugs, constructive pericarditis, pancreatitis, sepsis, etc.)
Clinical Findings
• Although clinical findings in shock vary according to the type of shock, clinical findings and pathophysiological changes are quite similar if left untreated. Shock may come with only tachycardia and tachypnea in the early period.
• Hypovolemic shock usually presents with altered mental status, tachypnea, tachycardia, hypotension, weak peripheral pulses, cold extremities, and oliguria. Supine hypotension and tachycardia are typical for hypovolemia. Dry mouth and decrease in turgor are observed.
• Septic shock has 2 phases:
1. Early or hot shock (characterized by low systemic vascular resistance).
2. Late or cold shock (characterized by high systemic vascular resistance).
• Septic shock may present in the early stages with warm extremities (due to peripheral vasodilation secondary to low systemic vascular resistance), pulsating pulses (due to high stroke volume and enlarged pulse pressure), tachycardia, tachypnea, adequate urine output, and mild metabolic acidosis.
• Cardiogenic shock presents with cold extremities, prolonged capillary refill time (>2-3 seconds), hypotension, weak peripheral and central pulses, tachypnea, clouding of consciousness, and oliguria (all findings are due to peripheral vaconstriction and decreased cardiac output).
• Decompensated shock, regardless of etiology, is a late-occurring condition characterized by hypotension, high vascular resistance, decreased cardiac output, changes in consciousness, and respiratory failure.
• Hemodynamic changes in different shock types are observed in the table.
• The transition from compensated to decompensated shock is not always easy to identify; however, increased lactic acid production and very low mixed venous oxygen saturation indicate tissue hypoxia and inadequate oxygen delivery, so these two findings are typical of decompensated shock. Although mixed venous oxygen saturation (SVO2 ) is best measured from the pulmonary artery catheter, in practice the most useful location is the measurement from the superior vena cava (SVCO2), as pulmonary artery catheters are rarely inserted in practice. Normal is 75-80%.
Treatment:
The ABCD step of resuscitation should be performed in all patients. (D-level is Dextrose in shock and should be remembered in the differential diagnosis of hypoglycemia)
• The first thing to do in the initial treatment of shock is to quickly give 20 ml/kg 0.9% NaCl (saline) or Ringer's lactate within 5-10 minutes. If vascular access cannot be established within 60 seconds or 3 attempts, intraosseous intervention is indicated for the patient.
• Depending on the patient's clinical response (such as regression in tachycardia, improvement in hypotension, shortening of capillary refill time, increase in urine output or improvement in consciousness), fluid boluses in the patient can be increased up to 60-80 ml/kg.
• In cardiogenic shock, fluid-filled bolus are performed with lower amounts (5-10 ml/kg). Dopamine or epinephrine can be started as inotropes. If perfusion disorder and acidosis persist due to increased systemic vascular resistance (SVR), although cardiac output improves, milrinone or dobutamine or nitroprusside can be added to the treatment. Drugs that increase SVR such as norepinephrine and vasopressin should not be used.
