Damage Control Resuscitation (DCR) is a systematic approach for managing major trauma patients at risk of exsanguinating hemorrhage. It incorporates permissive hypotension to minimize blood loss while hemorrhage is uncontrolled, haemostatic resuscitation using blood products instead of crystalloids to prevent coagulopathy, and early hemorrhage control through surgery. DCR aims to decrease mortality and morbidity by recognizing patients at risk of hemorrhagic shock, providing adequate tissue oxygenation through hypotensive resuscitation while limiting further blood loss and clot disruption, and preventing the triad of hypothermia, acidosis and coagulopathy through haemostatic resuscitation and blood product administration according to a
* Fluid resuscitation is mandatory in shock from traumatic haemorrhage * Massive use of resuscitative fluids following injury is now being disputed * Adequate resuscitation is no longer judged by presence of normal vital signs * Normalcy of organ and tissue specific measured values are to be achieved * Search for a single endpoint that works for all trauma patients, is unrealistic * Resuscitate with appropriate fluid, in appropriate amount, at appropriate time
* Fluid resuscitation is mandatory in shock from traumatic haemorrhage * Massive use of resuscitative fluids following injury is now being disputed * Adequate resuscitation is no longer judged by presence of normal vital signs * Normalcy of organ and tissue specific measured values are to be achieved * Search for a single endpoint that works for all trauma patients, is unrealistic * Resuscitate with appropriate fluid, in appropriate amount, at appropriate time
ATLS is two days course for those who manage trauma patients. These protocols have been followed by hospitals all over the world to treat trauma patients quickly and efficiently.
ATLS is two days course for those who manage trauma patients. These protocols have been followed by hospitals all over the world to treat trauma patients quickly and efficiently.
POLYTRAUMA AND DAMAGE CONTROL ORTHOPAEDICSDr Slayer
polytrauma is Injury to 2 or more organ systems leading potentially to a life threatening condition
Damage control orthopaedics is an approach to contain and stabilize an orthopaedic injury to improve patient’s physiology which are designed to avoid worsening pt’s condition due to “second hit” phenomenon
External ear,tympanic membrane and auditory tube Dr.N.Mugunthan.M.S.,mgmcri1234
External ear,tympanic membrane and auditory tube - Lecture by Dr.N.Mugunthan.M.S.,Associate Professor, Mahatma Gandhi Medical College & Research Institute, Pondicherry,
Sri Balaji Vidyapeeth University.
its sometime difficult to decide in urgent clinical scenarios - Trauma,active bleeding, surgery: What ; when ; how and why to transfuse? answering some of these queries here is my presentation especially made for PG students (will help in answer writing)
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
Anti ulcer drugs and their Advance pharmacology ||
Anti-ulcer drugs are medications used to prevent and treat ulcers in the stomach and upper part of the small intestine (duodenal ulcers). These ulcers are often caused by an imbalance between stomach acid and the mucosal lining, which protects the stomach lining.
||Scope: Overview of various classes of anti-ulcer drugs, their mechanisms of action, indications, side effects, and clinical considerations.
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
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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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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Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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
2. Damage Control Resuscitation
• Definition:
• A systematic approach to major exsanguinating trauma
incorporating several strategies to decrease mortality and
morbidity:
1. Permissive hypotension
(Minimal Normotension)
2. Haemostatic resuscitation
(Massive Transfusion Protocol)
3. Haemorrhage Control
(Damage control surgery)
3. Trauma Patient Mortality
• Head injury
= leading cause of death
(largely determined at the time of
Injury)
• Haemorrhagic Shock
= leading preventable
cause of death in trauma
4. Causes of Shock in Trauma
• Hypovolaemic
• Haemorrhage
• Obstructive
• Tension PTX
• Cardiac tamponade
• Distributive
• Neurogenic / Spinal
• Cardiogenic
• Direct cardiac contusion
5. Cause of Haemorrhagic Shock
• Direct Tissue Damage
• Dysruption of blood vessels with associated blood loss enough to cause
tissue hypoperfusion
• Coagulopathy
Intrinsic Factors
• Trauma Induced Coagulopathy (TIC) / Acute Coagulopathy of Trauma
(ACT)
• 10-40% of trauma patients
• Presence associated with 4-5 x increased mortality
Extrinsic Factors
• Hypothermia
• Dilution (crystalloids, blood components)
• Acidosis / Tissue Hypoperfusion
6. Trauma Induced Coagulopathy
(TIC):
• Definition:
• Intrinsic dysregulation of the blood coagulation in the
setting of trauma
• Pre-requisistes:
• Tissue Hypoperfusion
• Physical Tissue Damage
• Factors released by the tissue and endothelium in
response to injury and hypoxia cause coagulopathy by
several mechanisms:
• Anticoagulation
• Thrombin-thrombomodulin Protein C system dysfn
• Platelet dysfunction
• Hyperfibrinolysis
7. Principles of DCR
• Rapid Physical Control of Haemorrhage
• Provide adequate tissue oxygenation while reducing the
likelihood of UNCONTROLLED HAEMORRHAGE
• Recognise patients at risk of uncontrolled haemorrhage
• Introduce practices to reduce likelihood of:
• Clot rupture & Excessive blood loss
• Avoid “Excessive” intravascular pressures but maintaining
adequate tissue perfusion
= PERMISSIVE HYPOTENSION /
Minimal Normotension
• Coagulopathy
• Haemodilution
• Hypothermia
• Acidosis
= HAEMOSTATIC RESUS /
Massive Transfusion Protocol
8. Recognising patients at risk of
Uncontrolled Haemorrhage
• Clinically obvious / gestalt
• Scoring Systems:
• Trauma Associated Severe Haemorrhage (TASH) Score:
• SBP < 100 mmHg
• HR > 120 bpm
• HB < 70 g/l
• Positive EFAST with haemodynamic instability
• Pelvic / long bone fracture
• BE <-10 mmol/L
• INR >1.5
• Assessment of Blood Consumption (ABC) Score
• SBP < 90 mmHg
• HR >120 bpm
• Penetrating Mechanism
• Positive FAST
Score 2 = 38%, 3 = 45%, 4 = 100% chance of massive transfusion
• Thromboelastography / Coagulation testing
9. Prehospital Goals
(Where trauma centre available)
1. Control Haemorrhage
2. Rapid transport to trauma centre (definitive control)
3. Initiate resuscitation guided by:
• Mental status
• Peripheral pulses
• Consider delayed resuscitation (= nil resus fluids)
Studies in patients with penetrating trauma needing
thoracotomy have shown a 2.63x increased risk of death
with each prehospital procedure performed
10. Initial Mx in Trauma Centre
• Activation of trauma team
• on or prior to arrival
• Gen Surg / Anaes / ICU / Ortho / Blood Bank / Radiology
• Primary survey (ABC’s)
• Exclude early life threats (tamponade, tension PTX…)& establish
presence or risk of HAEMORRHAGIC SHOCK
• Manage Haemorrhage (immediate & plan definitive)
• Resuscitate patient (DCR)
• Usually all happen concurrently
• Secondary Survey (may not get to this)….
11. Haemorrhage Mx
• Localise source/s
• Clinical / imaging
• Initial control / minimise bleeding
• Pressure / Splinting / Traction /
Tourniquet….
• DCR
• Plan for early definitive Mx of haemorrhage
12. DCR Evidence
• What we know!
• Shock = BAD
• Longer the period of Shock = Worse
• Haemorrhaging trauma patients develop coagulopathy
• What we are still trying to work out?!
• How do we BEST maximise tissue perfusion without
exacerbating haemorrhage and coagulopathy
• Evidence = limited but developing
• anecdotal / animal studies / human retrospective & RCT’s
13. The Evidence:
Permissive Hypotension
• Multiple animal studies
• Reliable rebleeding point in pigs at SBP 94mmHg
• Hypotensive pigs aggressively resucitated (80ml/kg crystalloids)
• 3 x blood loss & greatly increased mortality compared with nil resucitation
• Review of fluid resus in animals (Mapstone) – Permissive Hypotension vs Normotension
• RR death 0.37 in permissive hypotension group
• Anecdotal / Retrospective
• WWI / WWII / Vietnam War
• Resuscitation in absence of bleeding control can be harmful
• Human Studies
• Penetrating torso with BP<80 mmHg RCT (Houston): Delayed vs Immediate resus
• Delayed: lower mortality (30% vs 38%), less crystalloids (375ml vs 2.5L, nil diff in MAP)
• Hypotensive trauma patients RCT : SBP target 70mmHg vs 100mmHg
• No change in mortality (ie. No increased mortality)
• Note no sig diff in SBP in the 2 groups
• Evidence suggests effect the same for Blunt & Penetrating
14. Permissive Hypotension Goals
• When to implement:
• While there is, or the potential for, uncontrolled haemorrhage
• Not when there is controlled haemorrhage (goal is normotension)
• How:
• Titrate small bolus (250ml) fluid administration to a hypotensive goal:
• SBP of 70-90mmHg OR
• normal mentation and palpable peripheral pulse (~radial
>80mmHg, ~brachial >60mmHg)
• Consider fentanyl bolus to prevent hypertensive episodes
• Aim is to prevent clot dislodgement / decrease rate of blood loss in the
immediate period after trauma, while maintaining “adequate” end
organ perfusion
• Use in head injury is controversial
• Some groups aim for normotension
• Some advocate increased BP goals >100 mmHg
• Some suggest nil change to other cases of haemorrhagic shock pt’s
15. Haemostatic Resuscitation
Causes of coagulopathy in trauma
• Haemodilution:
• Iatrogenic Dilutional
• excessive / any crystalloid use
• Physiologic Dilutional (extracellular fluid shifts)
• Acidosis
• pH<7.1-7.2 impairs thrombin prodn
• Hypothermia
• Impairs thrombin prodn & platelet fn
• <33°C causes ~20%loos of coag fn
• Hypocalcaemia – citrate poisoning due to massive transfusion
• Acute Traumatic Coagulopathy (ATC)
• Occurs if extensive tissue damage & hypoperfusion
• ?increased Activated Protein C
• Inactivates factors Va & VIIIa
• Promotes fibrinolysis
• Functionally decreases thrombin
16. Haemostatic Resuscitation:
The Evidence
• Massive transfusion protocol
• Multiple studies show increased survival
• Higher crystalloid use >mortatlity
• Higher ratio of FFP : RBC increased survival
• More recent wars (Afghanistan)
• Tranexamic Acid (TXA)
• CRASH 2 (2010, 20000 patients, RCT)
• Antifibrinolytic
• TXA increased survival, no increase in thrombotic episodes
• Recombinant Factor VIIa
• Recent Cochrane review found no improvement in mortality
17. Haemostatic Resuscitation:
Prevent / reduce coagulopathy
• Identify at risk group & act before coagulopathy develops:
• Massive transfusion protocol
• Early use of blood components as the primary resuscitation fluid
• Use in the same ratio as they are lost through haemorrhage
(exact ratio’s controversial)
• PRBC : FFP 1:1
• PRBC : Platelet (adult dose) 4:1
• Fibrinogen
• Give TRANEXAMIC ACID
• Prevent hypothermia / significant acidosis
• Monitor and give maintain iCa2+
18. Mx of Haemorrhagic Shock -
Crystalloids
• Historically resuscitation of trauma patients involved:
• RAPID restoration of circulating blood volume with
CRYSTALLOID SOLUTIONS to maintain normotension /
perfusion
• Advantages of crystalloids:
• Cheap
• Readily available / easy storage
• No risk of transfusion reactions / infectious agents /
hyperkalaemia / hypocalcaemia…
• The above Mx may be appropriate / not harmful in most
trauma patients
• But aggressive fluid resuscitation with crystalloids has
disadvantages!
19. Disadvantages of Crystalloids
• Increased Haemorrhage
• Coagulopathy (Haemodilution / hypothermia / acidosis)
• Clot rupture with restoration of normal blood pressure
• Compartment syndromes
• abdo, limbs
• Larger volumes needed when compared to blood products (3:1 rule)
• Lowers plasma osmotic pressures – more extravasation in damaged
areas (Hartmann’s worse than N Saline)
• Increased inflammatory repsonse
• Hartmann’s
• Acidosis
• N Saline
• Hartmann’s in those with impaired lactate metabolism (DKA, liver failure)
Aggressive use associated with increased mortality in haemorrhagic
shock
20. Haemostatic Resuscitation:
Blood Products
Volume (ml) Contents Grouping Storage
PRBC 200 50-70% HCT ABO & Rh 42 days
FFP 250-330 All coag factors
~1/2 unit WB
ABO 12 months
Platelets 100-400 200 x 109 Platelets
/ bag
ABO & Rh 5 days
Cryo 30-40 Firinogen / VIII /
XIII / VWF
~2 x unit WB
ABO 12 months
Whole Blood 24 hours
Remember:
•temperature
•citrate (hypoCa2+ after 4-6U PRBC in an hour)
•potassium
21. Haemostatic Resuscitation
Whole Blood Component Therapy
(1 PRBC / 1 FFP / 1 PLAT / 1
CRYO)
RBC (HCT) 38-50% 20%
COAGS 100% 50-60%
PLATELETS 150-400 X 103 / ul 280 x 103 / ul
FIBRINOGEN 1500mg 750 - 3000mg
Volume 450ml ~700ml (more with
flush)
22. Damage Control Resuscitation
(in a patient with haemorrhagic shock that cannot be
controlled in the ED)
• Permissive Hypotension
• No head injury
• Goal = SBP 70-90 mmHg (MAP 50-65) OR normal
mentation & peripheral pulses
• Head injury
• Controversial
• Some suggest permissive hypotension is
contraindicated
• Goal = normotension (depends on patient)
• Others use standard permissive hypotension
• Others adjust goal to SBP >100 mmHg
23. Damage Control Resuscitation
(in a patient with haemorrhagic shock that cannot be
controlled in the ED)
• Haemostatic Resuscitation
• If blood available:
• Initiate massive transfusion protocol
• Fixed product ratio’s
• Blood / FFP / Platelets / cryoprecipitate / calcium
• Monitoring of coagulation
• If blood not immediately available:
• Give 250-500ml boluses of crystalloids until blood available or resus goals met
• Warm Fluids / Cover Patient
• TXA
• give early (best <3/24) once risk of haemorrhagic shock determined
• 1g Stat and 1g over 8/24
• Relative contraindications: thrombophilic disorder
• Early definitive control of bleeding
• Consider rVIIa?
• If fibrinogen and platelets in sufficient numbers
26. The Future
• CryoStat
• Consensus on blood product use:
• Accurate bedside monitoring of Coagulation
parameters to guide blood product use
• Thromboelastography - ROTEM
27. Summary
• Identify those with / at risk of haemorrhagic shock on arrival
• Fluid resuscitation individualised for each patient
• Permissive hypotension in patients without head injury
• Early use of blood products as resus fluids
• Massive transfusion protocol – with fixed product ratios
• Monitor coagulation
• Use TXA in all patients requiring transfusion for uncontrolled
haemorrhage
• Early definitive Mx of haemorrhage
• Once haemorrhage controlled – then aim for normal CV
parameters
• monitor lactate / BE
28. Difficulties
• Alcohol / drug affected patients
• Head injured patient
• Delayed transfer to definitive care
• Complications of massive transfusion
29. References
• Bickell WH, Wall MJ Jr, Pepe PE, et al.: Immediate versus delayed fluid resuscitation for
hypotensive patients with penetrating torso injuries. N Engl J Med 1994, 331:1105-1109.
• Kaweski SM, Sise MJ, Virgilio RW, et al.: The effect of prehospital fluids on survival in trauma
patients. J Trauma 1990, 30:1215-1218.
• Kowalenko T, Stern SA, Dronen SC, Wang x: Improved outcome with hypotensive
resuscitation of uncontrolled hemorrhagic shock in a swine model. J Trauma 1992, 33:349-
353
• Alberto S. Santibanez-Gallerani, M.D., Annabel E. Barber, M.D., Shelley J. Williams, M.S.,
Yan Zhao, B.S., G. Tom Shires, M.D. Improved Survival with Early Fluid Resuscitation
Following Hemorrhagic Shock. World J. Surg. 25, 592–597, 2001
• Pek Ghe Tan, Marion Cincotta, Ornella Clavisi, Peter Bragge, Jason Wasiak, Loyal
Pattuwage and Russell L Gruen. Review article: Prehospital fluid management in
traumatic brain injury. Emergency Medicine Australasia (2011) 23, 665–676
• Philip F Stahel, Wade R Smith, Ernest E Moore. Current trends in resuscitation strategy for
the multiply injured patient. Injury, Int. J. Care Injured (2009) 40S4, S27–S35