Pediatric shock can be septic, cardiogenic, hypovolemic, distributive, or obstructive based on the underlying pathophysiology. Septic shock can present as warm shock with increased cardiac output and decreased systemic vascular resistance or cold shock with decreased cardiac output. Early recognition and treatment is key to managing shock. Treatment involves fluid resuscitation, inotropic support, and addressing the underlying cause of shock according to institutional guidelines. Differentiating between septic and cardiogenic shock involves clinical assessment of signs and symptoms as well as generating a therapeutic plan.
Anaphylaxis in children and adolescents-one-year survey in an immunoallergy d...Natacha Santos
Santos N, Gaspar A, Piedade S, Santa-Marta C, Pires G, Sampaio G, Borrego LM, Arêde C, Morais-Almeida M, Anaphylaxis in children and adolescents: one-year survey in an Immunoallergy department. Allergy 2012;67(Suppl.96):154.
In the medical community, summertime involves a unique set of medical issues along with an increase in trauma patients. First responders must be prepared to treat these patients quickly and efficiently so that morbidity and mortality can be minimized.
Lauren Mutter, MD, is a pediatric emergency medicine fellow at Le Bonheur Children's Hospital.
Mark Meredith, MD, is associate professor of pediatric emergency medicine at Le Bonheur Children's Hospital.
GEMC - Gastrointestinal Bleeding in the Pediatric PatientOpen.Michigan
This is a lecture from the Ghana Emergency Medicine Collaborative (GEMC). To download the editable version (in PPT), to access additional learning modules, or to learn more about the project, see http://openmi.ch/em-gemc. Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution Share Alike-3.0 License: http://creativecommons.org/licenses/by-sa/3.0/.
Educative power-point presentation for students in paediatrics, paediatric critical care, neonatology, And trainees or fellows in paediatric critical care
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Integrating Ayurveda into Parkinson’s Management: A Holistic ApproachAyurveda ForAll
Explore the benefits of combining Ayurveda with conventional Parkinson's treatments. Learn how a holistic approach can manage symptoms, enhance well-being, and balance body energies. Discover the steps to safely integrate Ayurvedic practices into your Parkinson’s care plan, including expert guidance on diet, herbal remedies, and lifestyle modifications.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
ABDOMINAL TRAUMA in pediatrics part one.drhasanrajab
Abdominal trauma in pediatrics refers to injuries or damage to the abdominal organs in children. It can occur due to various causes such as falls, motor vehicle accidents, sports-related injuries, and physical abuse. Children are more vulnerable to abdominal trauma due to their unique anatomical and physiological characteristics. Signs and symptoms include abdominal pain, tenderness, distension, vomiting, and signs of shock. Diagnosis involves physical examination, imaging studies, and laboratory tests. Management depends on the severity and may involve conservative treatment or surgical intervention. Prevention is crucial in reducing the incidence of abdominal trauma in children.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
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Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
2. Objectives
• By the end of this workshop, the learner will be
able to:
• Differentiate between septic and cardiogenic
shock states according to clinical assessment
and evaluation
• Generate a therapeutic/diagnostic plan
according to institutional and SCCM guidelines
where applicable
3. What is shock?
a. BP less than 5th percentile of age normal
b. Uncontrolled fluid loss/blood loss
c. Tachycardia and hypotension
d. Acidosis and increased lactate
e. Signs of organ dysfunction with decreased
UOP, altered mental status, etc.
4. Pediatric Shock
• Definition – what it is and what it is not
• Pathophysiology
• Recognition – early is key!
• Management- guidelines
• Case scenarios
• Ask for references, and you shall receive
6. Pediatric shock
• Cellular pathology
• Has nothing to do with blood pressure (until very late),
cardiac output, heart rate
• Inability to meet the metabolic demands (=oxygen) of the
tissue – or inability of the cell to use oxygen
• Supply-demand imbalance
7. What is shock?
• A hemodynamic abnormality that leads to inability to meet
tissue metabolic demands.
• Dynamic, progressive.
• A systemic reduction in tissue perfusion decreased
tissue O2 delivery.
• A shift to anaerobic metabolism
• Less efficient – 20-fold less ATP generated
• Leads to lactic acidosis
• Over time, progresses to,
• Cell membrane ion pump dysfunction
• Cellular edema, leakage of cells’ contents
• Inadequate regulation of intracellular pH
• Cell death, organ failure, cardiac arrest, and death.
9. Vocabulary
• CO –cardiac output
• CI cardiac index – CO indexed to BSA
• SVR, SVRI - systemic vascular resistance
• PVR,PVRI – pulmonary vascular resistance
• MAP – mean arterial pressure
• CVP – central venous pressure
• SV – stroke volume
• PAP – pulmonary artery pressure
• DO2 – oxygen delivery
• VO2 – oxygen consumption
10. Vocabulary - II
• CO – cardiac output: volume of blood ejected by the heart
in one minute 4-8 L/min
• Heart rate
• Stroke volume
• Contractility
• Afterload
• Preload
• SVR = MAP – CVP / CO
11. Oxygen Delivery – DO2
• Oxygen delivery= CO X CaO2 (Arterial oxygen content)
• CO=Heart rate X Stroke volume
• Stroke volume depends on preload, afterload and
contractility
•Arterial Oxygen content (CaO2) =
Hb x Sa02 x 1.34 +(0.003 x Pa02)
12. Oxygen Consumption – VO2
• VO2 = CO x (CaO2 – CvO2)
• Under normal conditions DO2 >> VO2 (physiological
reserve) – this is why you can exercise and don’t die
18. Shock – signs and symptoms
• Evidence of end organ hypoperfusion
• Decreased urine output
• Altered mental status
• Poor peripheral perfusion
• Metabolic dysfunction
• Lactic acidosis
• Altered metabolic demands
19. Shock: Feel the feet, look at the neck
• Tachycardia? - Non-specific, but early
• Skin changes? - Prolonged cap refill (vasoconstriction) with
compensated shock. Flash refill with early distributive shock and with
irreversible shock.
• Pallor? – If Hb is fine, is your patient acidotic
• Impaired mental status? – Fussy, irritable? Sleepy?
• Oliguria? – When was the last diaper?
• Hypotension? – You have missed the ball
• Widened pulse pressure (>40 mmHg)? - distributive shock, aortic
insufficiency, AVMs?
20. Compensatory Mechanisms
• Baroreceptors-In aortic arch and carotid sinus, low MAP
cause vasoconstriction, increases BP, CO and HR
• Chemoreceptors- Respond to cellular acidosis, results in
vasoconstriction and respiratory stimulation
• Renin Angiotensin Aldosterone - Decreased renal
perfusion leads to angiotensin causing vasoconstriction
and aldosterone causing salt and water retentions
• Humoral Responses-Catecholamines
• Autotransfusion-Reorientation of extravascular fluid
21.
22. Stages of Shock
• Compensated Shock:
• Cardiac output (HR x SV) and systemic vascular resistance (peripheral
vasoconstriction) work to keep BP within normal limits.
• Tachycardia; decreased pulses & cool extremities in cold shock; flushing
and bounding pulses in warm shock; oliguria; may have mild lactic acidosis
• Uncompensated Shock:
• Compensatory mechanisms are overwhelmed.
• Hypotension, altered mental status; increased lactic acidosis
• Generally quick progression to cardiac arrest.
• Irreversible Shock:
• Irreversible organ damage, cardiac arrest, death.
26. Classifications of Shock
• Hypovolemic Shock
• Decreased preload due to
internal or external losses.
• Distributive Shock
• Decrease in SVR, with
abnormal distribution of
blood flow functional
hypovolemia, decreased
preload.
• Typically, NL or CO.
• Cardiogenic Shock
• “Pump failure.” CO,
systolic function.
• Obstructive Shock
• Outflow from left or
right side of heart
physically obstructed.
30. Type of shock Mechanism of
circulatory failure
Signs and
symptoms
Interventions
Hypovolemic Volume depletion
absolute or relative,
CO ↓, SVR ↑
Tachycardia,
diminished pulses,
sunken eyes and
fontanels, oliguria,
prolonged cap refill
time
Crystalloid bolus 20
ml/kg until
hemodynamics
improve, reassess
after each bolus,
blood products in
hemorrhagic shock
Cardiogenic CO ↓, SVR ↑ Tachycardia,
diminished pulses,
hepatomegaly, JVD
Inotropic agents
dopamine,
dobutamine,
epinephrine,
milrinone
Small volume
boluses 5-10 ml/kg
might be
administered
carefully while
monitoring response
Get echo early
Consider PGE
31. Type of shock Mechanism of
circulatory failure
Signs and
symptoms
Interventions
Distributive
Anaphylactic
Neurogenic
CO ↑, then ↓, SVR
↓↓
Angioedema,
respiratory distress,
stridor, wheezing,
early hypotension
Start adrenergic
support while giving
fluids, obtain
vascular access
early,
supratherapeutic
doses of inotropes
might be required
CO normal, SVR ↓ Hypotension in the
absence of
tachycardia
Support SVR with
vasopressors,
phenylephrine might
be required, give
fluids as necessary
Obstructive Preload ↓, CO ↓,
SVR normal to ↑
Tachycardia,
hypotension, JVD,
tracheal deviation if
pneumothorax,
equalization of
pressures with
elevated CVP if
invasive monitoring
in place
Rapidly fatal if
underlying process
not recognized and
reversed, fluid
boluses should be
given while
preparation is made
for emergent
drainage
32. Type of shock Mechanism of circulatory
failure
Signs and symptoms Interventions
Septic “Warm shock”
CO ↑, SVR↓
Tachycardia, bounding
pulses, warm extremities with
hypotension, hyperpnoea,
altered mentation
Crystalloid boluses of 20
ml/kg repeat until
hemodynamics stable, first
choice agents vasopressors
(dopamine or norepinephrine)
“Cold shock”
CO ↓, SVR ↑
(60% of pediatric cases)
Tachycardia, poor peripheral
perfusion, diminished pulses,
hyperpnoea, altered
mentation
Crystalloid boluses of 20
ml/kg, repeat until
hemodynamics stable, early
inotropic support with
dopamine or epinephrine
might be required,
echocardiography might be
useful to guide therapy
CO ↓, SVR ↓ Tachycardia, diminished
pulses, with hypotension,
hyperpnoea, altered
mentation
Crystalloid boluses of 20
ml/kg repeat until
hemodynamics stable, early
inotropic support with
dopamine or epinephrine
might be required,
echocardiography might be
useful to guide therapy
34. What is the goal of shock treatment ?
•Optimizing oxygen content of the
blood
•Improving volume and distribution of
cardiac output
•Reducing oxygen demand
•Correcting metabolic derangements
35. Treatment
• Overall goal: Normalization of tissue perfusion and
homeostasis
• A - airway
• Secure, patent
• Oxygen administration – 100% FiO2 (except in some cases of
cardiogenic shock)
• B - breathing
• Decrease WOB, intubation-mechanical ventilation may be
necessary (decrease oxygen consumption)
• C - circulation
• Improve cardiac output
• Ensure adequate preload – FLUIDS!!!
36. Treatment - II
• Have I mentioned fluids?
• Give lots of fluids – fast!
• Then – give some more –up to 200 ml/kg may be required
• REASSESS! (After every step/intervention)
• Pay attention to hepatomegaly, JVD, rales, worsening
respiratory distress – if your patient is not responding to
the fluids, reconsider your diagnosis
• Once you reach 60 ml/kg, consider starting vasoactive
infusions –more on this later
37. Treatment - III
• D – “derangements”
• Correct metabolic abnormalities – hypoglycemia, hypocalcemia, etc
• Etiology specific treatment
•DO NOT DELAY ANTIBIOTICS FOR
ANY REASON IF YOU SUSPECT
SEPTIC SHOCK !
• Source control
• Consider transfusion of PRBCs
38. Assessing efficacy of treatment
• Blood pressure: Normal *
• Quality of central and peripheral pulses: Strong, distal
pulses equal to central pulses.
• Skin perfusion: Warm, with capillary refill 1-2 seconds.
• Mental status: Normal.
Urine output: >1 mL/kg per hour, once effective
circulating volume is restored.
39. Sepsis
• High mortality despite improvements
• KID database : 4.2% in all-comers, 2.3% in previously
healthy, 7.8% in chronically ill
• Guidelines are not effective unless protocol driven
• Early intervention is critical – no delay is acceptable.
• Every hour spent without reversing shock increases OR of
mortality
40.
41. SIRS SEPSIS SEVERE
SEPSIS
SEPTIC SHOCK
T > 38.5 or < 36
Tachycardia
Tachypnea
WBC
SIRS +
Infection
(suspected or
proven)
SEPSIS +
CV dysfunction or
ARDS or
≥ 2 organ failures
SEPSIS +
CV dysfunction
despite >40 ml/kg
in 1 hr
2 of the above 4
66. Ischemic Heart Disease in Children
• ALCAPA
• Anomalous Left Coronary Artery arising from the Pulmonary
Artery
• Kawasaki Disease
• Aneurysms
• Other vasculitis
67.
68.
69.
70. Treatment
• Support the failing pump
• Decrease oxygen consumption/metabolic demand
• Intubation*, mechanical ventilation
• Sedation, NMB
• Prevention of fever, stress
• Consider bolus 5-10 ml/kg
• Consider PGE
• Echo early
71. Treatment - II
• Optimize contractility
• Correct metabolic derangements
• Inotropic support
• Afterload reduction
• Decongestion
• Address the underlying cause – surgery?
• Mechanical support
• ECMO
• Implantable devices, VAD, EXCOR, etc
72.
73.
74. Type of shock Mechanism of
circulatory failure
Signs and
symptoms
Interventions
Hypovolemic Volume depletion
absolute or relative,
CO ↓, SVR ↑
Tachycardia,
diminished pulses,
sunken eyes and
fontanels, oliguria,
prolonged cap refill
time
Crystalloid bolus 20
ml/kg until
hemodynamics
improve, reassess
after each bolus,
blood products in
hemorrhagic shock
Cardiogenic CO ↓, SVR ↑ Tachycardia,
diminished pulses,
hepatomegaly, JVD
Inotropic agents
dopamine,
dobutamine,
epinephrine,
milrinone
Small volume
boluses 5-10 ml/kg
might be
administered
carefully while
monitoring response
Get echo early
Consider PGE
75. Question
• 13 month old patient with DCM, HR 180 (sinus), CVP 25
mm Hg, BP 55/24, lactate 4->8, SvO2 50%, cap refill of 5
seconds, best choice of action is:
a. Epinephrine gtt
b. Milrinone gtt
c. Phenylephrine gtt
d. NS bolus 20 ml/kg
e. Esmolol (B-blocker) for HR control
76. Question
• 12 year old female presents with fever, tachycardia, right
flank pain, WBC count is elevated. Vital signs are HR 155,
RR 35, BP 124/73, T 102. She is somnolent. Working
diagnosis is sepsis secondary to pyelonephritis. What is
the next most appropriate intervention?
A. Renal US
B. Normal saline bolus
C. Antibiotics
D. Vasopressor infusion
E. Urinalysis
77. Question
• 12 year old female presents with fever, tachycardia, right
flank pain, WBC count is elevated. Vital signs are HR 110,
RR 25, BP 124/83, T 102. She is AAO x 3 and is .
Working diagnosis is sepsis secondary to pyelonephritis.
What is the next most appropriate intervention?
A. Renal US
B. Normal saline bolus
C. Antibiotics
D. Vasopressor infusion
E. Urinalysis
78. Case 1
• 15-year-old male is just transferred to 11 WT from PICU, POD #3
from partial small bowel resection after multiple gunshot wounds
to the abdomen. The nurse calls an RRT because his HR has
increased in the last hour from 90 to 130, despite pain score of
1/10 on morphine drip. On exam, he is afebrile, HR is 140, BP
80/50. Cap refill is >3 seconds in his cool extremities and pulses
are 1+.
• What is your assessment?
• What is the stage of shock?
• What is the classification of shock?
• What is your initial management?
79. Case 2
• 6-year-old previously healthy girl is transferred from West
Campus ER with fever, bloody diarrhea x 1 day. She’s had no
urine x 24 hrs and is becoming harder to awaken. On exam, her
HR is 152, BP 72/32, temp 103. She’s sleepy but arousable.
She’s flushed with capillary refill <1 second.
• What is your assessment?
• What is the stage of shock?
• What is the classification of shock?
• What is your differential for the etiology?
• What is your initial management? If a higher level of care is needed,
how would you obtain it?
80. Case 3
• 4-month-old boy former premie, presents to ED with decreased po
x 2 days with 2 times daily emesis, following what sounds like viral
URI. Urine output has been 3 wet diapers daily. He is afebrile
with HR 180; BP has not been obtained. He has a weak cry, is
mottled with 3-second capillary refill, pulses 1+ in all extremities.
Liver is palpable 4 cm below RCM. S4 is present without murmur.
• What is your assessment?
• What is the stage of shock?
• What is the classification of shock?
• What is your differential for the etiology?
• What is your initial management?
81. What is the end goal for resuscitation ?
• Mixed venous sats
• Lactate clearance
• Traditional clinical variables –
UOP, perfusion, pulses, CVP
• Combination of all three with common sense
Teacher’s GuideReferenced above: Watson RS et al. The epidemiology of severe sepsis in children in the United States, Am J Respir Crit Care Med 2003; 167:695. Bone, RC. Toward an epidemiology and natural history of SIRS (systemic inflammatory response syndrome). JAMA 1992: 268:3452.
Teachers’ Guide:(This represents hypovolemic shock.)Example questions and examples of acceptable answers: What is your assessment?15 year-old post-operative patient with sudden tachycardia and borderline low blood pressure with impaired peripheral perfusion. Suggests hypovolemic shock.2) What stage of shock? Compensated … for now, given his lack of hypotension by strict definition. Given rapidity of onset, be extremely cautious for rapid decline.3) What classification of shock? If uncertain, what additional information would you want to obtain to decide?Hypovolemic shock, likely due to blood loss related to surgery; less likely septic shock (though you would be suspicious of this given the nature of his wounds) due to his physical exam findings. What is your initial management.Again, ABCDs, fluid resuscitation with 20 ml/kg crystalloid as needed to restore perfusion and blood pressure. Ensure a type and screen/cross match has been done and order PRBCs to the bedside in the event that bleeding continues. Stat baseline hemoglobin/hematocrit with repeat every 4 hrs until stable.MAIN TEACHING POINT: Hypovolemic shock is often first manifest by tachycardia and decreased peripheral perfusion. Hypotension is a late finding and indicates uncompensated shock.
Teachers’ Guide:(This represents cardiogenic shock.)Example questions and examples of acceptable answers: What is your assessment? 4 mo old with subacute onset of decreased desire to feed, emesis in setting of viral symptoms and possibly decreased urine output. Afebrile on exam with tachycardia and signs of hypoperfusion and liver distension and gallop. Suggests cardiogenic shock.2) What stage of shock? Answer is unclear given lack of available BP reading, but exam with impaired perfusion (and weak cry possibly indicating altered mental status) would suggest progression toward uncompensated shock.3) What classification of shock? If uncertain, what additional information would you want to obtain to decide?Likely cardiogenic, given decreased desire to feed, emesis, impaired perfusion, distended liver, and S4. Additional information could be gained through CXR looking for cardiac enlargement and pulmonary edema, stat echo, lactate, possibly chemistry looking for acidosis due to hypoperfusion and electrolyte imbalances due to emesis, +/- BNP. What leads your differential for the etiology?Given recent viral illness, viral cardiomyopathy possible cause. What is your initial management?ABCDs, continuing to monitor blood pressure closely and ensuring sufficient access, 10 ml/kg bolus (repeated with caution and constant monitoring for worsening heart failure, as needed) to restore perfusion if altered mental status or other signs of end organ dysfunction. Stat cardiac echo (or at least bedside ultrasound). Dopamine stat to the bedside. Stat cardiology consultation.MAIN TEACHING POINT: Cardiogenic shock is marked by decreased peripheral perfusion due to decreased cardiac output. Despite increased preload in cardiogenic and obstructive shocks, fluid boluses may be needed to restore perfusion if signs of end organ dysfunction. Howerver, because patient may worsen with these boluses the volume should be small and re-evaluation should occur after each intervention.