This document discusses principles of damage control resuscitation for traumatic hemorrhage. It describes how hemorrhage can lead to hypovolemic shock and coagulopathy, exacerbating blood loss. Damage control resuscitation aims to rapidly restore blood volume while limiting blood pressure increases to prevent further bleeding. It emphasizes early use of blood products rather than crystalloids to avoid dilutional coagulopathy, and maintaining hemostasis through permissive hypotension, tranexamic acid, and ratio-based blood component resuscitation. While controversial, this approach may improve outcomes compared to aggressive crystalloid resuscitation in severely bleeding trauma patients.
* 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
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)
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 Coagulopathy of Trauma: A Review of MechanismsEmergency Live
Coagulopathy associated with traumatic injury is the result of multiple independent but interacting mechanisms. Early coagulopathy is driven by shock and requires thrombin generation from tissue injury as an initiator. Initiation of coagulation occurs with activation of anticoagulant and fibrinolytic pathways.
Dr Sachin Gupta an intensivist at Peninsula Health presents on the difficulties we currently face in predicting bleeding and how this might change in the future.
Assessment and management of shock in acute trauma setting based on ATLS recommendations .Lecture given in Trauma update at Perintalmanna on19th August 2014.
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
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.
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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!
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
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.
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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2. IS IT IMPORTANT TO OUR
PRACTICE?
• Traumatic injury is the
leading cause of death in
under 45s
• Most victims are young
males
• Most preventable deaths
are due to haemorrhage
- leading preventable
cause of death in trauma
3. CAUSES OF SHOCK IN
TRAUMA
• Hypovolaemic Shock - haemorrhage (accounts
for ~40% of all trauma-associated deaths)
• Obstructive Shock - Cardiac Tamponade,
Tension Pneumothorax
• Distributive shock - Neurogenic/Spinal
• Cardiogenic - direct cardiac contusion
4. HAEMORRHAGIC SHOCK
• Hemorrhagic shock is a condition of reduced
tissue perfusion, resulting in the inadequate
delivery of oxygen and nutrients that are
necessary for cellular function. Whenever
cellular oxygen demand outweighs supply,
both the cell and the organism are in a state
of shock.
5. WHAT CAUSES
HAEMORRHAGIC SHOCK?• Direct Tissue Damage
• Disruption of blood vessels with associated blood loss can be enough to cause
tissue hypoperfusion
• Coagulopathy
• Intrinsic - Trauma-Induced Coagulopathy (TIC)/Acute Coagulopathy of Trauma
(ACT)
• Extrinsic
• Hypothermia
• Dilutional (administration of crystalloids/blood products)
• Acidosis/Tissue Hypo-perfusion
6. WHAT IS DAMAGE
CONTROL
RESUSCITATION?• A treatment strategy that targets conditions that exacerbate
haemorrhage in trauma patients
1. Find the bleeding, Stop the bleeding
1. Recognise the risk of an uncontrolled haemorrhage +/-
activation of Massive Transfusion Protocols
2. Restore blood volume rapidly and effectively (Permissive
Hypotension) - maximise tissue perfusion whilst minimising clot rupture and excessive blood loss
3. Maintain bloods function by maintaining the blood composition
(Haemostatic Resus) - haemostasis, oxygen-carrying capacity, oncotic pressure, biochemistry
7. WHAT IS DAMAGE
CONTROL
RESUSCITATION?• A treatment strategy that targets conditions that exacerbate
haemorrhage in trauma patients
1. Find the bleeding, Stop the bleeding
1. Recognise the risk of an uncontrolled haemorrhage +/-
activation of Massive Transfusion Protocols
2. Restore blood volume rapidly and effectively (Permissive
Hypotension) - maximise tissue perfusion whilst minimising clot rupture and excessive blood loss
3. Maintain bloods function by maintaining the blood composition
(Haemostatic Resus) - haemostasis, oxygen-carrying capacity, oncotic pressure, biochemistry
8. SCORING SYSTEMS• Trauma-Associated Haemorrhage Score
• M or F
• Hb (<70g/L +8, >120g/L 0)
• Base Excess (< -10mmol/L = +4, >-2mmol/L = 0)
• SBP ( <100mmHg = +4, >120mmHg = 0)
• HR (>120bpm = +2, <120bpm = 0)
• Positive FAST scan for intraabdominal fluid = +3
• Clinically Unstable Pelvic Fracture = +6
• Open or Dislocated Femoral Fracture = +3
• Assesment of Blood Consumption (ABC)
Score
• SBP <90mmHg
• HR >120bpm
• Penetrating Mechanism
• Positive Fluid on FAST Exam
• Score of 4 predicts 100% need for massive transfusion, Score of 3 predicts 45%
• McLaughlin Score
• HR >105bpm
• SBP <110mmHg
• pH <7.25
• Hct <32%
9.
10.
11. WHAT IS DAMAGE
CONTROL
RESUSCITATION?• A treatment strategy that targets conditions that exacerbate
haemorrhage in trauma patients
1. Find the bleeding, Stop the bleeding
1. Recognise the risk of an uncontrolled haemorrhage +/-
activation of Massive Transfusion Protocols
2. Restore blood volume rapidly and effectively (Permissive
Hypotension) - maximise tissue perfusion whilst minimising clot rupture and excessive blood loss
3. Maintain bloods function by maintaining the blood composition
(Haemostatic Resus) - haemostasis, oxygen-carrying capacity, oncotic pressure, biochemistry
12. WHAT IS DAMAGE
CONTROL
RESUSCITATION?• A treatment strategy that targets conditions that exacerbate
haemorrhage in trauma patients
1. Find the bleeding, Stop the bleeding
1. Recognise the risk of an uncontrolled haemorrhage +/-
activation of Massive Transfusion Protocols
2. Restore blood volume rapidly and effectively (Permissive
Hypotension) - maximise tissue perfusion whilst minimising clot rupture and excessive blood loss
3. Maintain bloods function by maintaining the blood composition
(Haemostatic Resus) - haemostasis, oxygen-carrying capacity, oncotic pressure, biochemistry
13. PERMISSIVE
HYPOTENSION: THE
EVIDENCE• “Injection of a fluid that
will increase blood
pressure has dangers in
itself. … If the pressure is
raised before the
surgeon is ready to
check any bleeding that
might take place, blood
that is sorely needed
may be lost.”
• — Walter Cannon, 1918
Walter Bradford Cannon
15. PERMISSIVE
HYPOTENSION: THE
EVIDENCE• Mapstone J, Roberts I, Evans P. Fluid resuscitation strategies: a
systematic review of animal trials. J Trauma. 2003 Sep;55(3):571-
89. Review. PubMed PMID: 14501908.
• Meta-analysis of animal trials
• 44 trials comparing fluid vs no fluid resus
• Fluid resuscitation appears to reduce the risk of death in animal
models of severe haemorrhage, but increases the risk of death in
those with less severe haemorrhage.
• Excessive fluid resuscitation could therefore be harmful in some
situations.
• Hypotensive resuscitation reduced the risk of death in all the trials
investigating it.
16. PERMISSIVE
HYPOTENSION: THE
EVIDENCE• Bickell WH, Wall MJ Jr, Pepe PE, Martin RR, Ginger VF, Allen MK, Mattox
KL. Immediate versus delayed fluid resuscitation for hypotensive
patients with penetrating torso injuries. N Engl J Med. 1994 Oct
27;331(17):1105-9. PubMed PMID: 7935634. [Free Full Text]
• non-blinded, semi-randomised prospective study
• n=598 adults with penetrating torso injury and SBP <90mmHg
• immediate resuscitation group (even days), delayed resuscitation group (odd days) - resus. started in OR, not
ED
• immediate resus (average 870ml) - isotonic crystalloid as per local paramedical protocol and ongoing isotonic
crystalloid infusion in ED
• delayed resus (average 92ml) - delayed any fluids/blood products until theatre.
• Outcome: mortality benefit favouring delayed resuscitation: 70% vs 62% (p=0.04)
• Comments:
• high-volume trauma centre in Houston - short door-to-theatre times
• patients were usually young and fit
• high potential for bias - not blinded, not randomised
• Crystalloid was used - not haemostatic resuscitation
• lacks external validity to settings where delayed presentation or blunt trauma predominates
• did not include TBI
17. PERMISSIVE
HYPOTENSION: THE
EVIDENCE
• Dutton RP, Mackenzie CF, Scalea TM. Hypotensive resuscitation
during active hemorrhage: impact on in-hospital mortality. J
Trauma. 2002 Jun;52(6):1141-6. PubMed PMID: 12045644.
• RCT with n=110
• titrating intial fluid therapy to SBP 70mmHg vs 100mmHg during active haemorrhage until
haemostasis
• no difference in mortality
• comments:
• small study with heterogenous patients - mostly young males, 51% penetrating trauma
• BP was similar in both groups regardless of the BP targets (suggests physiological adaptation
was occurring)
18. PERMISSIVE
HYPOTENSION: THE
EVIDENCE• Bjoern Hussmann, Matthias Heuer, Rolf Lefering, Alexander Touma, Carsten
Schoeneberg, Judith Keitel, and Sven Lendemans. Prehospital Volume Therapy
as an Independent Risk Factor after Trauma. BioMed Research International
Volume 2015, Article ID 354367, 9 pages http://dx.doi.org/10.1155/2015/354367
• Trauma Register of German Trauma Society - anonymous and standardised
multicenter database of severely injured patients. Since 1993.
• Restrospective analysis
• Patients between 2002 - 2010 with following criteria
• Primary admission to hospital (no transfers)
• Injury Severity Score (ISS) >/=16
• Age >/= 16 years
• Data available for prehospital and hospital volume therapy, PRBC
administration, GCS, Hb conc, base excess, one coagulation parameter, BP at
accident site, blunt trauma, therapeutic measures (resus, intubation, chest
tube insertion) and prehospital time
19. PERMISSIVE
HYPOTENSION: THE
EVIDENCE• Prehospital Volume Therapy as an Independent Risk Factor after
Trauma.
• 7,641 cases met the criteria and assigned to 1 of 5 groups - 0 -
500mL, 501 - 1000ml…>2001mL
• increasing volume groups correlated with male, car/MBA, prehospital
intubation, adrenaline, chest tube insertion
• Mortality: group 1: 18.3%, group 5 24.0%; p<0.01
• Conclusions: Prehospital volume therapy in patients without severe
TBI represents an independent risk factor for mortality
• Limitations:
• Anonymized data - could not access patient files for further
analysis
• Retrospective analysis - only associations and not causalities can
be ascribed
21. PERMISSIVE
HYPOTENSION:
TREATMENT PRINCIPLES• When to use it
• Uncontrolled Haemorrhage (or potential for it)
• Not in controlled haemorrhage (Where goal is normotension)
• Controversial in Head injury - Cerebral hypoperfusion
• some suggest aim for normotension
• some suggest SBP>100mmHg
• How to apply it
• Small boluses (250ml) of fluid to a hypotensive goal (SBP 85
- 100mmHg or MAP>65mmHg) + good radial pulse + pulse-
oximetry
• If the BP is too high, use titrated aliquots of Fentanyl (e.g
25mcg IV)
22. WHAT IS DAMAGE
CONTROL
RESUSCITATION?• A treatment strategy that targets conditions that exacerbate
haemorrhage in trauma patients
1. Find the bleeding, Stop the bleeding
1. Recognise the risk of an uncontrolled haemorrhage +/-
activation of Massive Transfusion Protocols
2. Restore blood volume rapidly and effectively (Permissive
Hypotension) - maximise tissue perfusion whilst minimising clot rupture and excessive blood loss
3. Maintain bloods function by maintaining the blood composition
(Haemostatic Resus) - haemostasis, oxygen-carrying capacity, oncotic pressure, biochemistry
23. HAEMOSTATIC
RESUSCITATION:
PRINCIPLES OF
MANAGEMENT
• Identify at risk group as early as possible
- Massive Transfusion Protocol
• Early use of blood components as the
primary resuscitation fluid instead of
crystalloid/colloids
• Use in the same ratio as they are lost
through haemorrhage (Exact ratios are
controversial)
• PRBC:FFP:Platelets 1or2:1:1
• Give Tranexamic Acid
• Prevent hypothermia
• Prevent acidosis
• Monitor and maintain Ca2+
24. HAEMOSTATIC
RESUSCITATION:
PRINCIPLES OF
MANAGEMENT
• Identify at risk group as early as possible
- Massive Transfusion Protocol
• Early use of blood components as the
primary resuscitation fluid instead of
crystalloid/colloids
• Use in the same ratio as they are lost
through haemorrhage (Exact ratios are
controversial)
• PRBC:FFP:Platelets 1or2:1:1
• Give Tranexamic Acid
• Prevent hypothermia
• Prevent acidosis
• Monitor and maintain Ca2+
25. CRYSTALLOIDS
• The Good
• Cheap
• Readily available
• Easily stored
• No risk of transfusion
reactions/BBV
• The Bad
• Increased haemorrhage -
increased clot rupture with
restoration of normal BP
• Dilutional coagulopathy
• Dilutional anaemia - impaired
oxygen delivery
• Hypothermia
• Metabolic Acidosis (N. Saline)
• Lowers plasma oncotic pressures -
haemodilution
The Bottom Line:
May be appropriate/not harmful in many trauma patients but aggressive
use is associated with increased mortality in haemorrhagic shock
26. HAEMOSTATIC
RESUSCITATION:
PRINCIPLES OF
MANAGEMENT
• Identify at risk group as early as possible
- Massive Transfusion Protocol
• Early use of blood components as the
primary resuscitation fluid instead of
crystalloid/colloids
• Use in the same ratio as they are lost
through haemorrhage (Exact ratios are
controversial)
• PRBC:FFP:Platelets 1or2:1:1
• Give Tranexamic Acid
• Prevent hypothermia
• Prevent acidosis
• Monitor and maintain Ca2+
27. HAEMOSTATIC RESUS:
THE PROPPR TRIAL
• PROPPR Study Group*, JAMA.
2015;313(5):471-482 Transfusion of Plasma,
Platelets, and Red Blood Cells in a 1:1:1vs a
1:1:2 Ratio and Mortality in Patients With
Severe Trauma
• 1:1:1 (intervention) vs 2:1:1(control) ratio in pt with severe trauma
and predicted to require MTP
• RCT. Treating clinicians were non-blinded.
• 12 North American Level 1 trauma centre sites
• Sample size 680 pts
28. PROPPR OUTCOMES
• Primary outcome - no significant difference in mortality at 24hours or at 30 days
• Authors Conclusions - Among patients with severe trauma and major bleeding, early
administration of plasma, platelets, and red blood cells in a 1:1:1 ratio compared with a 1:1:2
ratio did not result in significant differences in mortality at 24 hours or at 30 days.
• Strengths:
• Randomised, multi center
• Minimal loss to follow-up
• Weaknesses:
• unblinded
• 30 day max follow-up time
• study was powered to detect an absolute difference of 10% mortality - unable to detect a
smaller effect - 2968 patients would have been required to detect the observed difference of
4.2% (24 hour mortality) with 90% power
• Bottom line:
• no difference in 1:1:1 vs 2:1:1 ratio - although study was underpowered for the observed
difference
• 1:1:1 resulted in reduced mortality from exsanguination within the 1st 24 hours
29.
30. WHAT CAUSES
HAEMORRHAGIC SHOCK?• Direct Tissue Damage
• Disruption of blood vessels with associated blood loss can be enough to cause
tissue hypoperfusion
• Coagulopathy
• Intrinsic - Trauma-Induced Coagulopathy (TIC)/Acute Coagulopathy of Trauma
(ACT)
• Extrinsic
• Hypothermia
• Dilutional (administration of crystalloids/blood products)
• Acidosis/Tissue Hypo-perfusion
31. TRAUMA-INDUCED
COAGULOPATHY• Trauma-induced coagulapathy (TIC) and Acute Traumatic Coagulopathy
(ATC)
• “not simply a dilution coagulopathy or consumptive coagulopathy”
• Characterized by
• Isolated factor V inhibition - functionally decreases thrombin
• Dysfibrinogenaemia
• Systemic Anticoagulation
• Impaired platelet function
• Hyperfibrinolysis
• Exacerbated by
• hypothermia
• acidosis
• resuscitation by hypocoagulable fluid
32. HYPOTHERMIA
• Severe hypothermia is associated with a high
mortality
• <35 deg - platelet dysfunction
• <33 deg - clotting enzyme synthesis/kinetics,
plasminogen activator
• Progressive delay in the initiation of thrombus
formation
• Causes
• Pre-hospital
• ED - resuscitation period
• Theatre - exposure of peritoneum, resus fluids
• Treat
• Warmed fluids
• Bair Hugger/warm blankets
• Minimise exposure
• Increase ambient temp.
• Continuous Temp. Monitoring
33. ACIDOSIS AND BASE
EXCESS
• Both are independent predictive factors of mortality and identify
anaerobic metabolism (tissue hypoperfusion)
• pH strongly affects activity of Factors V, VIIa and X
• Acidosis inhibits Thrombin generation
• pH<7.2 - decreased contractility and CO, vasodilation,
hypotension, bradycardia, dysrhythmias
• Lactate is demonstrated to have the best association with
hypovolaemic shock and death - useful marker as an endpoint of
resuscitation
34. TRAUMA TRIAD OF DEATH
• Hypothermia
• Decreased cardiac output
• Arrhythmias
• Decreased function of
coagulation factors and
platelets
• Acidosis
• reduced contractility,
bradycardia, dysrhythmias,
vasodilation, hypotension
• Decreased function of
coagulation factors and
platelets
35. TRANEXAMIC ACID
• TXA is an anti-fibrinolytic agent
• The effect of TXA on mortality in a bleeding
patient is time dependant - survival advantage if
given early
• CRASH2 Trial - Placebo vs (1g/10min +
1g/8hrs)
• Hospital Mortality within 4 weeks of injury
reduced with TXA (14.5% vs. 16%, p=0.0035)
• Death due to haemorrhage reduced with TXA
(4.9% vs. 5.7%, p=0.0077)
• No significant increase in clots (MI, CVA, PE)
(1.7% vs. 2.0%, p0.084)
• TXA = good.
36. CRYOPRECIPITATE
• Fibrinogen (plus platelets) is the
primary substrate for clot
formation
• Reduced fibrinogen levels
correlate with increased mortality
• If fibrinogen is <1.0g/L give
Cryoprecipitate
• Contains: Fibrinogen, Factor
VIII, vWF, Factor XIII
• There is research into factors predicting
hypofibrinogenaemia on admission of
trauma patients - triage revised trauma
scores(T-RTS)/ISS - watch this space
37. DAMAGE CONTROL
SURGERY
• Initial operation with
haemostasis and packing
• Transport to ICU to
correct hypothermia,
acidosis, coagulopathy
• Return to theatre for
definitive repair
39. THROMBOELASTOMETRY
(ROTEM)• Viscoelastic method for testing
haemostasis in whole blood - point of care
test
• Displays a reaction curve showing
elasticity over time when a clot forms and
dissolves
• Jury is still out. It has applications in liver
and cardiac surgery. At the moment,
limited evidence in it’s role during Trauma.
Some studies show reasonable sensitivity
and specificity in diagnosing Acute
Traumatic Coagulopathy (72.7%, 77.5%)
• Crit Care. 2015 Mar 23;19:97. doi: 10.1186/s13054-015-0823-y.
Detection of acute traumatic coagulopathy and massive transfusion
requirements by means of rotational thromboelastometry: an
international prospective validation study. Hagemo JS1,2, Christiaans
SC3,4, Stanworth SJ5, Brohi K6, Johansson PI7,8, Goslings JC9,
Naess PA10, Gaarder C11.
40.
41. TAKE HOME MESSAGES
• Identify those with/at risk of haemorrhagic
shock
• Stop the bleeding
• Permissive Hypotension (in patients without
head injury)
• Haemostatic Resuscitation - early use of
blood products - Massive Transfusion
Protocol
• Use TXA in all patients with uncontrolled
haemorrhage
• Correct the correctible - hypothermia,
electrolyte derangements
• Monitor
• Don’t delay definitive treatment - Damage
Control Surgery