INITIAL ASSESSMENT OF TRAUMA PATIENTS....(INSPIRED FROM CTLS AND ATLS GUIDELI...Prerna Biswal
THIS PRESENTATION WAS MADE AT IMA HOUSE IN BHUBANESWAR,ODISHA, BY DR.NIBEDITA PANI,HOD ,DEPT. OF ANAESTHESIOLOGY AND DR.PRERNA BISWAL,PG,ANAESTHESIOLOGY,SCBMCH,CUTTACK,
Shock: A review of hypovolemic, septic, cardiogenic and neurogenic shock.Joseph A. Di Como MD
A review of different types of shock encountered in patients. Hypovolemic, septic, cardiogenic and neurogenic shock. We review etiology, pathophysiology, diagnosis, treatment and how to differentiate between them.
Thyroid and its pathology (Hypothyroidism).Vikas Reddy
GREEK :- THYREOS – SHIELD ; EIDOS – FORM
1.LOCATION:- Anterior to trachea in between the cricoid cartilage and the suprasternal notch.
2.SHAPE:- It has 2 lobes connected with an isthmus, each lobe in turn has two poles.
3.Weighs around 10-20 gm, highly vascular and soft in consistency.
4. 4 Parathyroid glands which secrete PTH are located posterior to each pole of thyroid
The RLN traverse the lateral border of thyroid gland and must be identified during thyroid surgery to avoid injury and vocal cord paralysis.
Develops from the floor of primitive pharynx during the 3rd week of gestation.
Fetal cells in which developmental transcription factors TTF-1,TTF-2 & PAX-8 are expressed selectively form the thyroid gland ,secondly they result in induction of thyroid specific genes
Tg,TPO,NIS,TSH-R.
Mutations-THYROID AGENESIS & DYSHORMONOGENESIS(CONG. HYPOTHYROIDISM).
The developing gland migrates along the thyroglossal duct to reach its final location in the neck.
LINGUAL THYROID AND THYROGLOSSAL DUCT CYST.
Thyroid hormone synthesis begins at about 11 weeks of gestation.
Until 11 week of gestation and even later, it is the maternal thyroid hormones which cross the placenta to reach the fetus and aid its development.
Therefore a child born to a hypothyroid mother would suffer from features of congenital hypothyroidism.
Secondly if the mother has TSH-R blocking antibodies or has received anti thyroid therapy during pregnancy, might lead to transient congenital hypothyroidism.
INITIAL ASSESSMENT OF TRAUMA PATIENTS....(INSPIRED FROM CTLS AND ATLS GUIDELI...Prerna Biswal
THIS PRESENTATION WAS MADE AT IMA HOUSE IN BHUBANESWAR,ODISHA, BY DR.NIBEDITA PANI,HOD ,DEPT. OF ANAESTHESIOLOGY AND DR.PRERNA BISWAL,PG,ANAESTHESIOLOGY,SCBMCH,CUTTACK,
Shock: A review of hypovolemic, septic, cardiogenic and neurogenic shock.Joseph A. Di Como MD
A review of different types of shock encountered in patients. Hypovolemic, septic, cardiogenic and neurogenic shock. We review etiology, pathophysiology, diagnosis, treatment and how to differentiate between them.
Thyroid and its pathology (Hypothyroidism).Vikas Reddy
GREEK :- THYREOS – SHIELD ; EIDOS – FORM
1.LOCATION:- Anterior to trachea in between the cricoid cartilage and the suprasternal notch.
2.SHAPE:- It has 2 lobes connected with an isthmus, each lobe in turn has two poles.
3.Weighs around 10-20 gm, highly vascular and soft in consistency.
4. 4 Parathyroid glands which secrete PTH are located posterior to each pole of thyroid
The RLN traverse the lateral border of thyroid gland and must be identified during thyroid surgery to avoid injury and vocal cord paralysis.
Develops from the floor of primitive pharynx during the 3rd week of gestation.
Fetal cells in which developmental transcription factors TTF-1,TTF-2 & PAX-8 are expressed selectively form the thyroid gland ,secondly they result in induction of thyroid specific genes
Tg,TPO,NIS,TSH-R.
Mutations-THYROID AGENESIS & DYSHORMONOGENESIS(CONG. HYPOTHYROIDISM).
The developing gland migrates along the thyroglossal duct to reach its final location in the neck.
LINGUAL THYROID AND THYROGLOSSAL DUCT CYST.
Thyroid hormone synthesis begins at about 11 weeks of gestation.
Until 11 week of gestation and even later, it is the maternal thyroid hormones which cross the placenta to reach the fetus and aid its development.
Therefore a child born to a hypothyroid mother would suffer from features of congenital hypothyroidism.
Secondly if the mother has TSH-R blocking antibodies or has received anti thyroid therapy during pregnancy, might lead to transient congenital hypothyroidism.
Hyperthyroidism, Reference: Hyperthyroid, Harrison's Principles of Internal Medicine, Soheil Elahi, Islamic Azad University of Medicine- International Branch (IAUM-int)
د/باسم السيد
Management of shocked patient
المحاضرة التي قدمت يوم الثلاثاء 8 ابريل 2014 في دار الحكمة بالقاهرة
من فعاليات مشروع اعداد طبيب حكيم ناجح بالتعاون مع معتمد باتحاد الاطباء العرب
و ضمن موديول الطوارئ و التخدير و العناية المركزة
Simple medical student presentation about distributive shock, type and pathophysiology of each septic shock, anaphylactic shock, neurogenic shock
including management, prognosis and disposition of patient..
brief info of type of inotropes and when to start.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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
Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
263778731218 Abortion Clinic /Pills In Harare ,sisternakatoto
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
1. • References:
1. Sarawak Handbook Of
Medical Emergencies 3rd
Edition
2. Guide to The Essential in
Emergency Medicine by
Shirley Ooi.
3. Parrillo & Dellinger: Critical
Care Medicine, 3rd ed.
4. Civetta, Taylor, & Kirby's:
Critical Care, 4th Edition
5. http://www.cc.nih.gov/ccc/ped
web/pedsstaff/ivf.html
(Intravenous Fluid
Management)
Lim Jun Sian Batch
12
2. • Clinical syndrome that is results from
• Circulatory failure
• Reduction in oxygen deliver
• inadequate peripheral tissue and organ perfusion leading to a
• eventual cellular hypoxia with all its attendance sequalae.
• Clinically characterized by
• hypotension (Hemodynamic instability)
• SBP < 90mmHg or < 30mmHg from baseline
• Mean arterial pressure < 65mmHg
• Oliguria
• Altered mentation
• Organ failure
4. Pathophysiology
• resulting from a decreased circulating blood
volume
Types of Hypovolemia
• Blood Loss
• Fluids/Plasma Loss
Most common type of shock
Diagnosis
• Readily diagnosed based on the etiology
• Pitfall
• Difficult to differentiate from cardiogenic
• A normotensive patient maybe in shock ( hypertensive patient)
6. Class I Class II Class III Class IV
Blood loss
mL <750 750-1500 >1500-200 >2000
% <15 15-30 >30-40 >40
Heart rate
(beat/min)
<100 >100 >120 >140
Systolic
blood
pressure
Normal Normal Decreased Decreased
Pulse
pressure
Normal Decreased Decreased Decreased
Capillary
refill normal
Delayed Delayed Delayed Delayed
Respiratory
rate (min)
14-20 20-30 30-40 >35
Urine output
(mL/h)
>30 20-30 5-15 Minimal
7. • Cardiogenic shock (CS) is characterized by
systemic hypoperfusion due to
• cardiac pump failure caused by loss of myocardial
contractility
• severe depression of the cardiac index [<2.2 (L/min)/m2]
and
• sustained systolic arterial hypotension (<90 mmHg)
despite an elevated filling pressure [pulmonary capillary
wedge pressure (PCWP) >18 mmHg].
• Most common cause: MI
• 15% of cardiogenic shock occurs during MI attack
• 50% occurs 6 hours after MI attack
9. • Septic Shock:
• sepsis-induced hypotension (systolic blood pressure
<90 mm Hg [or a drop of >40 mm Hg]) with
• signs of tissue hypoperfusion
• despite adequate fluid resuscitation for at least 1 hour
• Refractory septic shock
• Septic shock that lasts for >1 h and does not respond to
fluid or pressor administration
• Principle of mechanism
1. Peripheral vasodilation and pooling of blood
10. • Symptoms:
FEVER/hypothermia,
depends on site of
infection.
• Signs:
• Warm peripheral
extremities (due to
vasodilation)
• Febrile
• hypotension
• Tachypnea, tachycardia
• Oliguria
• Rash
• History taking:
comorbidities
• DM,
• Chronic lung disease
• alcoholism,
• liver cirrhosis,
• Recent invasive
procedure (especially in
CKF)
• HIV
• Immunosuppressive agent
(Steroid)
• Malignancy
11. • An allergic, IgE mediated, hypersensitivity
response to a foreign substance to which a
patient has been previously sensitized
• Type I hypersensitivity
• Causes:
• Drugs: penicillin, aspirin, streptomycin
• Vaccines: measles
• Blood products
• Insect bites: bees
• Food: seafood
12. • Onset:
• Commonly: 5-60min of exposure
• Delayed onset: after few hours
• Biphasic response: recurrence of symptoms 1-8 hrs later
due to late phase reaction
• Protracted anaphylaxis : persistence of symptoms up to
48hrs despite therapy
• Skin :
• Urticaria (200 cases):Area of focal dermal edema
• angioedema (20cases): Localized non-pitting deeper
edematous process
• Pruritus
• Tingling of face (usually at mouth)
13.
14.
15. • CVS:
• Arrhythimias
• RS:
• Laryngeal edema: hoarseness of voice, stridor, “lump in
the throat”
• Wheeze
• Dyspnea due to bronchospasm
• Coughing: ominous sign portend onset of pulmonary
edema
• GIT
• Nausea, abdominal cramp
23. Hypovolemic Shock
Cardiogenic Shock
Obstructive Shock
Distributive Shock
Neurogenic Shock
Check the Pulse
Tachycardia
Dysrhythmia
s(by ECG)
Bradycardia
Neurogeni
c
AnaphylacticCardiogenicSepticHypovolemic
Other
Features:
Trauma
diarrhea
vomiting
Other
Features:
Fever
Rash
others
Other
Features:
Post – MI
Sign of CCF
Other
Features:
Allergy
Urticarial
angioedema
Other
Features:
Spinal
injury
RS
Examination
Tension
Pneumothor
ax
Cardiac
Tamponad
e
BECK’S TRIAD
24.
25. Airway Maintenance If GSC < 8 ETT intubation
Breathing – by SP02
100% oxygen
oyxgen to maintain PaO2 >
60mmHg or SaO2 > 90%
Circulation
2 large wide bore
• Size: 16G
• Route: peripheral
central line Intraosseos
line
• Wide bore
• Purpose:
• Give bolus or infuse
fluids
• Drugs administration
• blood Investigation
Bladder
catheterization
26. • Supine or
Trendelenburg
position
• Raise the leg up
Non-
cardiogenic
Shock
Cardiogenic
Shock
Fluids therapy
(at least
1000ml)
+/- Fluids
therapy (500-
1000ml max)
Investigation CVP or PAC
Fail to respond to Fluid therapy
Sympathomimeti
cs
• Mean arterial pressure >60-
65 mm Hg (higher in the
presence of coronary artery
disease)
• Pulmonary wedge pressure
15-18 mm Hg (may be higher
for cardiogenic shock)
• Cardiac index >2.1 L/min/m2
for cardiogenic and
obstructive shock
• Cardiac index >4-4.5
L/min/m2 for septic and
resuscitated
traumatic/hemorrhagic shock
29. • Crystalloid is preferred over than colloid because
colloid :
1. inhibition of the coagulation system;
2. the risk for anaphylactoid reactions;
3. inhibition of renal salt and water excretion;
4. Over-administration risk of ARF
5. expensive
30. • Choice of Crystalloid
• Theoretically: Ringer Lactate or Hartman solution is
preferred over Normal saline
• Resemble the plasma electrolytes level
• However, Normal saline is used because
• it is cheaper.
• Isotonic Normal saline 0.9% is used in all shock
condition excepts:
• Burn shock (use Parkland formula)
• Dextrose 5% ½ NS Maintenance therapy
31. 1. The value of Glucose, Na, K must be
memorized.
• Primarily used to
maintain water
balance in patients
who are not able to
take anything by
mouth
For Fluid Resuscitation
(shock, dehydration)
Fluids
Maintenance
33. Fluids loss
• Fluids replacement : (NS) to restore the
circulatory volume
• Adult: at least1000ml over 30minutes bolus
• Pediatrics – 20ml/kg
• Calculating the % loss
• According to the sign and symptom
• Dehyration – mild moderate severe
• Blood loss – class I,II, III, IV
• According to weight loss
• (Previous healthy weight – current body weight) x
100%
34. • Fluids maintenance: daily fluid loss (about 2L) +
additional fluid deficit + ongoing loss
• (fever –increase in 1degree celcius =10ml/hr
loss)
• Paediatrics age group – Must use Holliday-
Segard Formula
• Adult – can use wt + 40 formula
• Maximum fluid maintenance for normal daily loss
: 120ml/ hr
35. Rule of 4 -2-1 (Holliday-
Segard Formula)
- 4 ml per kg for the first 10
kg of body weight;
- 2 ml per kg for the next 10
kg (11-20kg);
- 1 ml per kg for any weight
>20 kg
Weight + 40
Example: Calculating
maintenance fluid
requirements for 70 kg male.
0-10 kg: 10 * 4 ml = 40 mL
11-20 kg: 10 * 2 mL = 20 mL
21-70 kg: 50 * 1 mL = 50 mL
Total = 110 mL/hr
Example: Calculating
maintenance fluid
requirements for 70 kg male.
70+40 = 110mL/hr
36. • Indications
• Severe hemorrhage > 30%
• Hb < 8%,
• Whole Blood is used.
• GXM
• 1 unit of blood = 450ml of blood
• During initial resuscitation of acute blood loss and shock,
crystalloid or colloid infused to restore circulatory volume
• Emergency blood group “O” blood should not be used
indiscrimately
• Look for side effect of transfusion
37. • Group O “positive” is used as emergency blood for man.
• Group O “negative” is used for female in reproductive
age group.
• Category of blood according to urgency
Unmatch
Emergency
blood
Rapid
Match
blood
Full
matched
blood
Availability Instant 5-10minutes 30-
45minutes
CXM not done done Done
Antibody
screen
not done not done done
Guide to The Essential in Emergency
Medicine by Shirley Ooi.
38. • Prevention of stress ulcer
• Ranitidine or PPI
• Prevention of deep vein thrombosis
• UF heparin or LMW heparin if no C/I
• Prevention of ARF
• Induce diuresis by furosemide (make sure adequate fluid
therapy) look for hyperkalemia
• IV 2-5micro g/kg/minute of dopamine (low dose)
• Glucose control
• Insulin to prevent DKA in DM patient
• Metabolic Acidosis
• treat in severe cases only.
39.
40. • Blood investigations
• FBC, RBS
• HCT is extremely unreliable test
• GXM
• BUSE and creatinine, lactate
• Cardiac enzyme and TnT
• Exclude acute MI
• ABG
• Metabolic acidosis, elevated lactate(>5mmol/L) and significant
base deficit are marker of poor prognosis
• Correction of these abnormalities will improve outcome (by ABC)
• However, sodium bicarnoate is not used routinely because it does little
to positively affect morbidity and survival.
• Coagulation profile , albumin
• ECG and CXR
• FAST scan (Focused assessment with sonography for trauma)
41. • Fluids
Resuscitation -
mainstay
• All fluids need to be
warmed to prevent
iatro-genically
induced
hypothermia.
ABC + Bladder
catheterization
Active
bleeding
Fluid
Resuscitatio
n
Dopamine
+/-
Dobutamine
Compressi
on
E / NE
HypotensionCVL / PAC
Hypotension
OT if
required
If MAP < 60mmHg
CVL / PAC
sympathomime
tic drugs
external
Internal
42.
43. • Blood Investigation
• Cardiac enzyme
• ABG
• BUSE and creatinine
• FBC , RBS
• ECG
• CXR
• Echocardiography if cause is uncertain
44. • Assessment of Venous Pressure:
reflect Right ventricular filling pressure
• Pulmonary capillary wedge pressure
(PCWP) with Swan-Ganz catheter
• useful in suspected ARDS, exclusion of
VSD, associated hypotension requiring
inotrope to guide therapy
45.
46. Supine or Trendelenburg position
ABC + bladder catheterization
Oyxgen 35-100% via facemask
to maintain PaO2 > 60mmHg or
SaO2 > 90%
Continuous cardiac, BP,
HR, Pulse oxymetry
monitoring
• Increase inspired
oxygen to keep
SaO2 > 90%
• Mechanical
ventilation is
indicated if
• hypercapnia
• hypoxia
• Patient who are alert
and cooperative may
cope with (NIPPV)
• Correct severe
metabolic acidosis
(pH < 7.2)
• Reason: negative
inotrophic and
pro-
47. Treat underlying arrhythmias
• Insert large cannula and
give:
• Morphine IV 2.5-5mg
+ metoclopramide
10Mg IV or IM
Reduce
anxiety and
vasodilation
(use carefully)
Notice: SL GTN
and frusemide
are not used in
Cardiogenic
Shock if SBP <
NO CLINICAL OR
HEMODYNAMIC PULMONARY
CONGESTION
• Look for sign of CCF
48. NO CLINICAL OR
HEMODYNAMIC
PULMONARY
CONGESTION
(Judicious fluid challenge)
Method of giving:
Without invasive
hemodynamic monitoring
• 100ml NS or
Hartman’s Solution
over 5-10min interval
• Reassessment of BP,
HR, peripheral
perfusion, breath
sound between
successive
administration
• Max : 500-1000mL
With invasive
hemodynamic monitoring
Investigation
as above
49. Still Hypotension
Dopamine
Peripheral
hypoperfusion and
significant hypotension
use dopamine
increase MAP + restore
renal and coronary
perfusion
Up to 15-20 µg/kg/min
Common desired effect
dosage: 7.5-15µg/kg/min
Contraindicated
Dobutamine
Contraindicated in significant
pulmonary congestion and only
mild hypotension
Still Hypotension
50. Still Hypotension
NE/E Phosphodiesteras
e –III inhibitors
OR
NE/E
NE: beta1 and alpha
adrenergic increase
contractility +
vasoconstriction
Use if dopamine fails
Caution: both are
proarrhythmias (if AMI
extensive myocardial
injury)
Phosphodiesterase –III
inhibitors
Eg. Amrinone and
milrinone
Indication: severe
Treat Pulmonary
Edema
With Frusemide /
GTN
SBP > 100mmHg
AMI if present
- Follow MI protocol
51. • Aminophylline (rarely use)
• Increase cardiac contractility
• Bronchodilatation
• Vasodilatation
• Mechanical circulatory support
• Intra-aortic balloon counterpulsation in tertiary
centers
• increases myocardial oxygen perfusion while
at the same time increasing cardiac output.
52.
53. • To establish the definitive diagnosis
•Blood Culture and sensitivity (2 sets)
• For IV line sepsis:1 set from suspected
IV line, another from peripheral vein
•Urine C&S
•Stool culture
•Sputum culture
•UFEME
56. ABC
Watch I/O
carefully and be
aware of other
losses
Continuous ECG, BP,
HR, Pulse oxymetry
monitoring
Bladder catheterization
Pulmonary arterial catheterization
57. Fluid Challenge
• Mainstay of
hemodynamic
supports
• Fast and rapid wide
bore fluid resuscitation
• urine output rate
should be kept at >0.5
mL/kg per hour by
continuing fluid
administration
• central venous
pressure should be
maintained at 8–12
cmH2O
Rate of administration
should be reduced if
cardiac filling
pressure increase
without concurrent
hemodynamic
improvement
58. Give low dose of
vasopressin
increase systemic
arterial pressure to
sustains the ability of
the vasculature to
autoregulate flow on a
tissue and organ level
prevent organ
failure
Low Dose
vasopressor
• NE /
Dopamine(not in
low dose) 1st
choice
• Alternate:
Epinephrine (if BP
is poorly
responds)
• Enhance sensitivity to
vascular smooth muscle to
catacholamine to
minimize the side effect of
using high dose vasopressor
• beneficial in catecholamine-
resistant septic shock
following adequate volume
59. • C&S before empirical antibiotic
• Intravenous broad-spectrum antimicrobials
should be initiated immediately (preferably <30
minutes) following the clinical diagnosis
• At dosing at the high end of the therapeutic
range
• Duration of therapy: 7-10 days
• Empiric antimicrobial therapy should be adjusted
to a narrower regimen within 48 to 72 hours if a
plausible pathogen is identified or patient
stabilizes clinically Where possible, early source
60. • Indications:
• Early phase of fibro-proliferative phase of ARDS
and sepsis
• History of endocrine disease and history of taking
corticosteroid therapy
• Persistent hypotension after adequate fluids
resuscitation and vasopressin
• Meta-analysis showed no convincing
evidence that early administration of high
dose corticosteroid is beneficial and they
could be harmful.
61. • Human recombinant activated protein C
(drotrecogin alfa)
• Indicated in high risk for death (APACHE II > 24 or
multi-organ failure
• Effect:
• Antithrombotic
• Anti-inflammatory
• Pro-frinolytic
• Prerequisite: Platelet count > 30,000
• Main contraindication
• Active bleeding
• CRF
62.
63. ABC
Bladder
catheterization
ECG,RR,BP,SaO2
recumbent position
• High flow Oxygen
with facemask fail
ETT difficult
intubation due to
severe laryngeal
edema
tracheastomy /
cricothyroidotomy
Remove the inciting agent
• Prompt application of
torniquet proximally
• Insect: flick out insect
stinger with a tongue
blade
• Ingestion of allergen :
gastric lavage and
activated charcoal
64. IM aqueous
epinephrine 0.3-
0.5 ml of 1:1000
Repeat every
20minutes
• Epinephrine is the
mainstay of initial
management
• controlling symptoms
and maintaining blood
pressure.
IV Epinephrine
3 – 5ml 1:10
000
Severe
airway
compromise /
hypotension
Repeat every 5-
10min
Epinephrine
Infusion
If require
multiple doses
65. Administer
histamine
antagonists
• block vasodilation,
capillary leak, and
shock
• H1 blockade, 25–50 mg
of diphenhydramine IV
6hrly
• ; H2 blockade, 50 mg of
ranitidine IV 6hrly
aggressive fluid
resuscitation
500-1000ml of
crystalloid or colloid
in patients
who remain
hypotensive
despite
epinephrine.
Still
Hypotension
67. • Nebulizer Bronchodilator
•Short acting beta2 agonist every 15-
30minutes
•Due to refractory to epinephrine
• Consider Corticosteroid
•250mg IV hydrocortisone, repeated 6
hourly
•Reduce protracted anaphylaxis
•not effective therapy for the acute
manifestations
68. • Consider glucagon administration
•Indicated for those who receive B blocker
therapy in anaphylactic shock
antagonizes the beneficial β-mediated
effects of epinephrine therapy
•1–5 mg IV over 1 minute, then 1–5
mg/hour in a continuous infusion
69. • Continuous ECG monitoring
• Close monitoring of ABG, CVP, BP
• Antihistamine 48-72hours to prevent
relapse
• Short course of steroid for 7-10 days
• Counseling
70. • Clinical features:
• Bradycardia, hypotension, warm peripheral
extremities
• Mx:
• ABC + Supine position with leg elevated
• Fluid resuscitation
• NE
• Anal wink or bulbocarvenosus reflex
Editor's Notes
(1) hypovolaemic, due to inadequate venous return (haemorrhage, dehydration), (2) cardiogenic, due to inadequate ventricular pump function (myocardial infarction), (3) obstructive, due to vascular obliteration (pulmonary embolism or tamponade), and (4) distributive, due to loss of vasoregulatory control (sepsis).
Atelectasis - Recumbency and involuntary restriction of ventilation secondary to pain reduce functional residual capacity and may lead to atelectasis
Shock and, in particular, resuscitation-induced oxidant radical generation, is recognized as a major cause of acute lung injury and subsequent acute respiratory distress syndrome (ARDS;
severe sepsis or septic shock may demonstrate persistent vasomotor dysfunction characterized by regional perfusion deficits with or without systemic hypotension despite normal or increased CO. Clinical manifestations may include lactic acidosis and ongoing progression of organ failure.
Acute Physiology and Chronic Health Evaluation
β-blockade antagonizes the beneficial β-mediated effects of epinephrine therapy, thereby resulting in unopposed α-adrenergic and reflex vagotonic effects: vasoconstriction, bronchoconstriction, and bradycardia