Presentation on theme: "START WITH THE NAME OF ALLAH. Approach to child with Shock & coma Dr Yasmeen Memon Associate Professor Paediatric Unit 1."— Presentation transcript:
START WITH THE NAME OF ALLAH
Approach to child with Shock & coma Dr Yasmeen Memon Associate Professor Paediatric Unit 1
Learning objectives After completion of this section the students should be able to: To know pathophysiology of shock To know common types of shock To know initial management of shock To identify causes of coma. Know how to investigate child with coma Know how to treat the child at health facility.
Facility Based Management The first step is, to assess referred case in the triage –where we screen the cases to decide to which of the following group(s) a sick child belongs: Those with emergency signs require immediate emergency treatment. Those with priority signs should alert you to for immediate assessment and treatment. Children with no emergency or priority signs are treated as non-urgent cases.
Shock Acute syndrome characterized by the body inability to deliver adequate oxygen to meet the metabolic demands of vital organs & tissues.
Pathophysiology An initial insult triggers shock, thus disrupting blood flow to end-organs, leading to inadequate tissue perfusion. Insufficient oxygen at tissue level ---shift of aerobic cellular metabolism to less efficient anaerobic metabolism - --- progressive lactic acidosis --- clinical deterioration The body's compensatory mechanisms are initiated to maintain perfusion to vital organs, leading to compensated shock. If inadequate tissue perfusion persist --- adverse vascular, inflammatory,metabolic,cellular,endocrine & systemic responses worsen the physiologic instability. If treatment is not introduced during this period of compensated shock, decompensated shock develops, causing tissue damage that leads to multisystem organ dysfunction and death
Child with Shock
Types of Shock Hypovolemic ---Decreased preload -- diarrhea, vomiting, hemorrhage. Cardiogenic ---Cardiac pump failure secondary to poor myocardial function-- CHD, acute myocarditis, cardiomyopathies. Septic ---Includes multiple forms of shock Hypovolemic:third spacing Distributive:early shock with decreased after load Cardiogenic:depression of myocardial function by endotoxins Bacterial,Viral,Fungal (immunocompromised patients are at increased risk)
Types of Shock Obstructive ---(:significant direct obstruction to right or left heart function, or restriction of all cardiac chambers --mechanical barrier impede cardiac out put) pericardial tamponade, tension pneumothorax, pulmonary embolism. Distributive --- inadequate vasomotor tone leads to capillary leak & mal-distribution of fluid into interstitium --- Anaphylaxis,Neurologic:loss of sympathetic vascular tone secondary to spinal cord or brainstem injury,Drugs
Clinical presentation The clinical presentation of shock depends, in part, on the cause; if shock is unrecognized and untreated, a very similar untoward progression of clinical signs and pathophysiologic changes occurs and leads to a common final path. The clinical features of shock also relate to the stage (duration vs progression) of the process (early vs late). All forms of shock affect heart rate—preload, afterload, or myocardial contractility—or a combination of all 3 components, leading to poor tissue perfusion. More than 1 of these processes may occur simultaneously
Hypovolemic shock usually presents as changes in mental status, tachypnea, tachycardia, hypotension, poor peripheral pulses, cool extremities, and oliguria. Supine hypotension and tachycardia are hallmarks of hypovolemia. Neonates and infants may also have poor urine output. Dry mucous membranes, dry axillae, and poor skin turgor are variably present. Hypovolemic shock may initially present with normal or only slightly cool distal extremities
Septic shock, in particular, has 2 phases: Early, or warm, shock is diagnosed by low SVR, and late, or cold, shock is diagnosed by high SVR. Septic shock may present initially with warm extremities (from peripheral vasodilation secondary to low SVR), bounding pulses (from high stroke volume and widened pulse pressure), tachycardia, tachypnea, adequate urination, and mild metabolic acidosis.
Cardiogenic shock presents with cool extremities, delayed (>2–3 sec) capillary filling time, hypotension, poor peripheral or central pulses, tachypnea, increasing obtundation, and decreased urination (all caused by peripheral vasoconstriction and decreased cardiac output
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,Enlarged 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
INITIAL MANAGEMENT The initial treatment in pediatric shock is to stabilize the ABCDs and provide appropriate fluid resuscitation The ABCs of resuscitation (airway, breathing, and circulation) must be evaluated and stabilized for all patients in shock. Neonates and infants in particular may also have profound hypoglycemia associated with shock; it maybe helpful to recognize the ABCDs, with the D standing for dextrose in the pediatric population. Once the patient's airway, breathing, circulatory access, and dextrose are stabilized, treatment specific to shock can be initiated
How to give IV fluids rapidly for shock in a child without severe malnutrition If the child is severely malnourished the fluid volume and rate are different, so check that the child is not severely malnourished Shock in child without severe malnutrition — ➤ Insert an intravenous line (and draw blood for emergency laboratory investigations). ➤ Attach Ringer's lactate or normal saline — make sure the infusion is running well. ➤ Infuse 20 ml/kg as rapidly as possible
Volume of Ringer's lactate or normal saline solution Age/weight (20 ml/kg) 2 months (<4 kg) 75 ml 2 – <4 months (4 – <6 kg) 100 ml 4 – <12 months (6 – <10 kg) 150 ml 1 – <3 years (10 – <14 kg) 250 ml 3 – <5 years (14 – 19 kg) 350 ml
Reassess child after appropriate volume has run in Reassess after first infusion: If no improvement, repeat 20 ml/kg as rapidly as possible. Reassess after second infusion: If no improvement, repeat 20 ml/kg as rapidly as possible. Reassess after third infusion: If no improvement, give blood 20 ml/kg over 30 minutes (if shock is not caused by profuse diarrhea, in this case repeat Ringer ’ s lactate or normal saline). Reassess after fourth infusion: If no improvement, see disease-specific treatment guidelines. You should have established a provisional diagnosis by now.
After improvement at any stage (pulse slows, faster capillary refill) Give 70 ml/kg of Ringer's lactate solution (or, if not available, normal saline) over 5 hours in infants (aged <12 months) and over 21/2 hours in children (aged 12 months to 5 years. Reassess the child every 1 – 2 hours. If the hydration status is not improving, give the IV drip more rapidly. Also give ORS solution (about 5 ml/kg/hour) as soon as the child can drink; this is usually after 3 – 4 hours (in infants) or 1 – 2 hours (in children). Reassess after 6 hours (infants) and after 3 hours (children). Classify dehydration. Then choose the appropriate plan (A, B, or C to continue treatment. If possible, observe the child for at least 6 hours after rehydration to be sure that the mother can maintain hydration by giving the child ORS solution by mouth.
If, after appropriate fluid resuscitation, the patient continues to show poor perfusion and shock, vasoactive agents are needed Septic, cardiogenic, distributive, and rarely, hypovolemic shock may require various drugs to stimulate heart rate (chronotropic) and cardiac contractility (inotropic) and enhance peripheral vascular resistance If the patient continues in a state of shock, inotropic support should be initiated. Dopamine is the 1st-line agent and should be quickly optimized before the initiation of other agents. 5–15 μg/kg/min Adequate infection therapy should also be provided for patients with septic shock; abscesses should be drained and appropriate bacteriocidal antibiotic therapy
Coma --- state of unconsciousness from which the child can not be aroused by ordinary verbal, sensory or physical stimuli
Child with coma
Diagnostic approach Coma is a medical emergency,life sustaining measures have precedence over diagnostic procedures The ABCs of resuscitation (airway, breathing, and circulation) must be evaluated and stabilized
Assessment of child with coma AVPU scale. Alert Response to vocal commands. Response to pain Un-conscious.
Stabilize and investigate CBC and MP CSF Blood glucose. Assessment of blood pressure Urine microscopy. Other investigations according to presentation ADMIT THE CHILD & MANAGE ACCORDINGLY
INPATIENT MANAGEMENT –HISTORY –DETAIL EXAMINATION & D/D –FOLLOW INVESTIGATIONS –NEED FOR FURTHER INVESTIGATION –MANAGE ACCORDINGLY
Approach to a child with Convulsion/lethargy/ unconsciousness History – determine if there is H/o Head trauma, drug over dose or toxin ingestion Convulsion – how long do they last? Past H/o febrile convulsions ? Infant < 1 wk – H/0 birth asphyxia, birth injury
Clinical Examination General – jaundice, Severe palmar pallor, peripheral edema, level of consciousness, petechail rash BP Stiff neck Sign of head trauma/ other injuries Pupil size & reaction to light Tense or bulging fontanelle Abnormal posture
Lab investigation LP ( if no sign of raised ICP) Blood smear in malarious area Blood sugar Urine microscopy
D/D of Convulsion/lethargy/ unconsciousness Causes Infaour Septic Meningitis History of high grade fever Recurrent history of otitis media Neck stiffness Signs of meningial irritation Petachial rashes (meningiococal meningitis) Tense or bulging fontenelle Abnormal posture CSF suggestive of septic meningitis
D/D of Convulsion/lethargy/ unconsciousness T.B meningitis H/o of contact with TB patient H/o of weight loss Low grade fever Loss of appetite Focal neurological signs Cranial nerve palsy Labs: CXR,Sputum AFB, mantoeux test,
D/D of Convulsion/lethargy/ unconsciousness Cerebral Malaria fever Jaundice Severe anemia Convulsion Blood smear positive for MP Hypoglycemia
Appearance of P. falciparum in thin blood films Ring forms or trophozoites; many red cells infected – some with more than one parasite
D/D of Convulsion/lethargy/ unconsciousness Acute gastro-enteritis with severe dehydration H/o loose motion & vomiting Sign of dehydration – sunken eyes, loss of skin turger, lethargy unable to drink or poor drinking
Testing Skin pinch for assessing dehydration
Sepsis Severely ill child Fever with no obvious focus of infection Negative blood smear for MP No neck stiffness or specific sign of meningitis Normal LP Sign of systemic upset (inability to drink or breast feed, convulsion,lethargy or vomit every thing) Purpura may be present
D/D of Convulsion/lethargy/ unconsciousness Head trauma Sign or H/o head trauma Poisoning. H/o poison ingestion or drug over dose PoisoningHx of poison ingestion or drug over dose
D/D of Convulsion/lethargy/ unconsciousness Hypertensive Encephalopathy H/o of head ache Vomiting Irritability Raised blood pressure
D/D of Convulsion/lethargy/ unconsciousness Diabetic ketoacidosis H/o of polydypsia, polyphagia, polyurea H/o of weight loss Acidotic breathing ( deep, laboured) Labs: High blood sugar Urinary ketones & sugar
D/D of Convulsion/lethargy/ unconsciousness Hypoglycemia (Always seek the cause i.e S. malaria & treat to prevent recurrence ) Blood glucose low & respond to glucose treatment
D/D of Convulsion/lethargy/ unconsciousness Shock – can cause lethargy or unconsciousness but is unlikely to cause convulsion Sign of shock Petechial rash Sign of severe dehydration
D/D of Convulsion/lethargy/ unconsciousness Acute glomerulonephritis with encephalopathy Raised BP Peripheral or facial edema Blood/protein/red cell casts in urine