Parker Flashcards
ASA Grades
1 - normal healthy individual
2- mild systemic disease that does not limit activity
3- severe systemic disease that limits activity but is not incapacitating
4- incapacitating systemic disease which is constantly life threatening
5- moribund, not expected to survive 24hrs with/without op
c.50% of elective patients = ASA 1
Op mortality = <1 in 10,000
POSSUM Scoring
Physiological and Operative Severity Score for the enUmeration of Mortality and Morbidity
developed in a general surgical pop and has been adapted for vascular, colorectal and oesophago-gastric patients
12 physiological and biochemical variables + 6 operative variables => estimated mortality risk
risk adjusted assessment of surgical quality and accurately predicts 30 day morbidity and mortality
Elective surgery grades
graded in accordance to the degree if stress it will cause
- Minor - e.g. excision of skin lesion
- Intermediate - e.g. inguinal hernia repair
- Major - e.g. hysterectomy
- Major plus - e.g. colonic resection
The FEV1/FVC ratio is the ratio of the forced expiratory volume in the first one second to the forced vital capacity of the lungs.
The normal value for this ratio is above 0.75-85, though this is age dependent.
<0.70 = airflow limitation = obstructive pattern
restrictive lung diseases often produce a FEV1/FVC ratio which is either normal or high with a reduced FVC
CV disease scoring e.g. Revised cardiac risk index
- High-risk surgery
- IHD
- Hx of CCF
- Hx of CVD
- Insulin therapy for GM
- Renal impairment
risk of major cardiac event 0.5% for zero points, 10% for more than 2 points
Risk factors for post op MreI
elective op should be deferred for 6mo post MI
Risk for post op re-infarction:
- Short time since previous infarct
- 0-3mo = 35%
- 3-6mo = 15%
- >6mo = 4%
- residual major coronary vessel disease
- prolonged/major surgery
- impaired myocardial function
c.60% post op MIs = silent
Mortality = c.40%
Complications associated with obesity:
- CV: HTN, IHD, CVD, DVT, difficult vascular access
- Respiratory: Difficult airway, difficult mechanical vent, chronic hypoxaemia, OSA, Pulmonary HTN, Post op Hypoxaemia
- Other: GORD, Abn liver runction, insulin resistance, T2DM, poor post op pain control, unpredictable pharmacological response
Complications associated with CKD:
- electrolyte disturbances
- impaired acid-base balance
- anaemia
- coagulopathy
- impaired autonomic regulation
- protection of veins, shunts, fistulas
When obstaining informed consent patients should be informed of:
- Detailed of diagnosis
- Uncertainties about the diagnosis
- Options available for treatment
- Proposed purpose of procedure
- Prognosis with and without procedure
- Likely benefits and probability of success
- possible side effects
- reminder that patient can change their mind at any stage
- reminder that patients have the right to a second opinion
All Qs should be answered honestly, info should not be witheld which might influence the decision, patient should not be coerced, person who obtains consent must be suitably trained and qualified, they must have sufficient knowledge of the proposed Rx and risks, good practice for this to be the physician provising the treatment
Consent forms 1-4
- Consent Form 1 - Patient agreement to investigation or treatment
- Consent Form 2 - Parental agreement to investigation or treatment
- Consent Form 3 - Patient/parental agreement to investigation or treatment (procedures where consciousness not impaired)
- Consent Form 4 - Form for adults who are unable to consent to investigation or treatment
Consent forms 5-9
- Consent Form 5 - Patient Agreement to Anti-cancer treatment
- Consent Form 6 - Supplementary Consent for Gifting of Tissue
- Consent form 7 - Consent to photography and conventional or digital video recordings form.
- Consent Form 8 - Consent for hospital post mortem examination on an adult
- Consent Form 9 - Consent for hospital post mortem examination on a baby or child
Consent in children
at 16yrs a child can be presumed to have capacity to decide on treatment
below the age of 16 a child may have the capacity to decide depending on their ability to undeerstand what the treatment involved (Gillick)
If a competent child refuses treatment a person which parental responsibility may authorise treatment which is in the child’s best interest
Mental capacity act
under the MCA a person is presumed to make their own decisions ‘unless all practical steps to help him/her have been taken without success.
Incapacity is not based on the ability to make a wise/sensible decision to determine
- is there an impairment or disturbance in the function of their mind/brain or an inability to make decision
A person is unable to make a decision is they:
- cannot understand the information relevant to the decision
- they are unable to retain that information
- they are unable to use/weigh that information as part of the decision making process
- they are unable to communicate the decision
If, having taken all practical steps to assist someone, it is concluded that a decision should be made for a person the decision must be made in that person’s best interest therefore…
- do not make assumptions on the basis of age, appearance, condition or behaviour
- consider all relevant circumstances
- consider whether/when the pt will have capacity
- support the pt’s participation in any acts/decisions made for them
- do not make a decision about life sustaining Rx motivated by a desire to bring about death
- consider the pts expressed wishes, feelings, beliefs, values
- take into account the views of others with an interest in the person’s welfare, their carers and those appt to act on their behalf
What risk assessment models fo you know?
- Goldman cardiac risk index
- parsonnet score
- POSSUM
- Injury severity score
- Revised trauma score
- APACHE I, II, III
WHO Safe surgery check list
- address preventable human error through a series of checks: sign in, time out, sign out, prior/during/after surgical procedure
- aims to strengthen the commitment of clinical staff to address safety issues within the surgical setting
- incl - improving anaesthetic safety practices, ensure correct site surgery, avoid surgical infections, improves communication within teams
- shown to reduce risk of complications and death
What is pharmacokinetics
study of the bodily absorption, distribution, metabolism and excretion of drugs
What is pharmacodynamics
study of the biochemical and physiological effects of drugs and their mechanisms of actions
General anaesthesia
drug induced state of unresponsiveness usually achieved by the use of a combination of agents
3 phases: induction, maintenance, reversal and recovery
GA: premedications
- Amxiolysis - benzodiazepines, phenothiazines
- analgesia - opiates, non-steroids anti-inflammatories
- Amnesia - benzodiazepines, anticholinergics
- Antiemetics - anticholinergics, antihistamines, 5HT antagnosits
- Antacids = alginates, PPIs
- Anti-autonomic - anticholinergics, B Blockers
- Adj - bronchodilators, steroids
Induction agents
IV, highly lipid soluble, rapidly cross BBB, distributed to organs with high bld flow e.g. brain, rapidly redistributed -> rapid onset/recovery
- thiopentone - short acting barbituate
- depresses myocardium and in hypovolaemic pt -> profound hypotension
- propofol - most commonly uses
- short 1/2 life, causes hypotension
- used as an infusion for maintenance
- no analgesic properties, used with opioids e.g. fentanyl
What is RSI
Rapid sequence induction = rapid induction of anaesthesia
Cricoid pressure -> reduces the risk of aspiration
pressure is released once definitive airway is achieved
e.g. thiopentone & suxamethonium
Pt who are not fastes/ Hx of GORD/Intestinal obstruction/pregnancy/intra-abdo pathology
Benefits/complications of ET airway
ET = placement of a tube into the trachea to maintain a patent airway
- Benefits:
- Protection against aspiration and gastric insufflation
- Effective ventilation and oxygenation
- Facilitation of suctioning
- Delivery of anaesthetic and other drugs
- Complications:
- Failed intubation -> hypoxaemia
- Right mainstem inbutation
- Oesophageal intubation
- trauma from laryngoscope to teeth/soft tissues
- Vocal cord damage
- Aspiration and post intubation pneumonia
- pneumothorax
- Hypotension and arrythmias
What are the 3 aspects of anaesthesia?
- Hypnosis - suppression of consciousness
- Analgesia - suppression of physiological responses to stimuli
- Relaxation - suppression of muscle tone and relaxation
Wha are the ideal features of an inhalational anaesthetic agent
inhaled volatile gases, lipid soluble hydrocarbons, high saturated vapour pressures
Potent, non-inflammable, non-explosive
- Easily administered
- boiling point above ambient temp
- low latent heat of vaporisation
- chemically stable with long shelf life
- compatible with soda-limb, metals, plastics
- non-flammable
- cheap
- Phamacokinetic
- low solubility
- rapid onset, offset, adj depth
- minimal metabolism
- predictable in all age groups
- Pharmacodynamic
- high potency- allows high FiO2
- High therapeutic index
- Analgesic
nb MAC - Minimal Alveolar Concentration = alveolar conc required to keep 50% of pop unresponsive
Halothane
potent anaesthetic but poor analgesic agent
MAC = 0.75
20% metabolised in liver
can cause hepatic dysfunction, occasionally causes severe hepatitis, can progress to liver necrosis
Depresses myocardial contractility and can induce arrythmias
Isoflurane
potent anaesthetic but poor analgesic agent
MAC = 1.05
Less cariotoxic than halothane
More resp depression than halothan
reduces peripheral resistance and can cause coronary steal
Few adverse effects reported
Nitrous oxide
Weak anaesthetic agent, cannot be used alone without causing hypoxia
potent analgesic agent
50% N2O/50%O2 = Entonox
Used in anaesthesia for it’s analgesic properties
What are the adverse effects of inhalation anaesthetic ?
- Cardiovascular:
- Decrease myocardial contractility
- reduced cardiac output
- hypotension
- arrhythmias
- Increased myocardial sensitivity to catecholamies
- Respiratory:
- depress ventilation
- laryngospasm and airway obstruction
- decrease ventilatory response to hypoxia & hypercapnia
- bronchodilatation
- CNS
- increase cerebral blood flow
- reduce cerebral metabolic rate
- increase risk of epilepsy
- increase iintracranial pressure
- Other
- decrease renal blood flow
- simulate nausea and vomiting
- precipirate hepatitis
GA: Muscle relaxants
either depolarising or non depolarising
Depolarising (e.g. suxamethonium)
- act rapidly within seconds and their effects last for c.5mins
- used during induction of anaesthesia
- SE:
- Histamine release = ‘scoline rash’
- Bradycardia
- Somatic pain from fasciculation
- Hyperkalaemia
- Increased intra-ocular pressure
- Increased gastric pressure
- Severe complications:
- 1:7000, persistent neuromuscular blockage -> ‘scoline apnoea’, due to pseudocholinesterase deficiency
- 1:100,000, increased Ca influx, uncontrolled metabolism -> increased Ca influx and uncontrolled metabolism -> increased body temp with increasing PCO2 -> Malignant hyperpyrexia
Non-depolarising (e.g. vecuronium) act over 2-3mins, effects last 30mins - 1hr, competitive antagonists of acetylcholine receptor, used for intra-op muscle relaxation
Anaesthetist - peri-op monitoring
- maintain the airway & oxygenation
- manual, guedel, LMA, ETT, Tracheostomy T
- preserve circulation
- prevent hypothermia
- prevent injury
- monitor during anaesthesia
e.g.:
- Always: Temp/HR/BP/ECG/O2 of inspiratory gas mix/Ent tital CO2/Pulse oximetry
- Consider: Invesive BP monitoring, Central venous pressure, Urine output
Arterial pressure monitoring
Requires:
- arterial cannula
- monitoring line
- transducer
- monitoring system
Provide info on systolic and diastolic pressure & arterial waveform
Complications/problems:
- Over and under dampening
- incorrect zeroing
- haematoma
- distal ischaemia
- inadvertent drug injection
- disconnection and haemorrhage
- infection
Central Venous Pressure
Cannulation of central venous system by internal jugular or subclavian routes -> more accurate info re CVP and intravascular volume (&cardiac pre-load)
Complications:
- pneumothorax
- arterial puncture
- air embolism
- infection
Swan-Ganz catheter
Balloon tipped catheter inserted through central vein, through right heart into pulmonary artery, bloon alow weding in a branch of the pulmonary artery = pulmonary capillary wedge pressure = left atrial pressure
Tip contains a thermistor
CO - measured using themodilution principal
Complications:
- arrhythmias
- knotting and misplacement
- cardial valve trauma
- pulmonary infarction
- pulmonary artery rupture
- balloon rupture
- catheter thrombosis or embolism
Primary haemodynamic date obtained from S-G includes:
- HR, MAP, CVP, Mean pulmonary artery pressure, mean pulmonary artery occlusion pressure, cardiac output, ventricular ejection fraction
Data derived from this:
- Cardiac index, stroke volume, stroke volume index, systemic vascular resistance, systemic vascular resistance index, pulmonary vascular resistance index, left ventricular stroke work index, right ventricular stroke work index, oxygen delivery, oxygen consumption
Recovery from anaesthesia: cause of failure to breath post anaesthetic
- obstruction of airway
- central sedation due to opiates/anaesthetic agent
- hypoxia
- hypercarbia
- hypocarbia due to overventilation
- persistent neuromuscular blockade
- pneumothorax
- circulatory failure leading to resp arrest
Common intra-operative nerve injuries?
- Ulnar nerve - resting arms in pronation alongside the patient (medial epicondyle and operating table)
- Brachial plexus - arms in abduction (>60) and external rotation
- Common peroneal nerve - lithotomy position (fibula head and table)
- Radian nerve - tourniquet/misplaced injection in deltoid muscle
Plasma
Fluid component of blood - 55%
pH 7.34-7.45
90% water, 10% solutes
Solutes = Albumin 60%, globulins 35%, fibrinogen, thrombin, hormones, chloesterol, nitrogenous wastes, nutrients, electrolytes
Erythrocytes
biconcave discs 7.5um in diameter
formed in bone marrow and removed from circulation in the liver/spleen
no nuclei or mitochondria
life span 120 days
red cell production requires: iron, amino acids, vitamins, hormones, - erythropoietin
Reticulocytes = immature red cells
1-2% of circ
Red cell production is stimulated by - H’gge, anaemia, hypoxia, increased O2 requirement
Leukocytes
1% of blood volume
nuclei and mitochondria
5 types:
- neutrophils 40-70%
- phagocytosis - bacteria
- lymphocytes 20-40%
- produced in LN/spleen
- B=antibodies, T=cell mediated immunity NK = immune surveillance
- monocytes 4-8%
- precursors of tissue machrophages
- basophils 1%
- histamine, chemotactic agents
- Eosinophils
- parasites, immune complex destruction
Platelets
fragments of megakaryocytes
bone marrow
life span = 10 days
granules contain; Ca, ADP, serotonin, platelet derived frowth factor
Role in blood coagulation
Iron Metabolism
Body contains c.5g of iron
65% of body’s iron is in Hb, 30% in ferritin and haemosiderin, 3% myoglobin
Daily dietary requirement = 1mg (man), 3mg (woman), average diet contains c.15mg, in ferric hydroxide and ferric-protein complexes e.g. liver and meat, c.5-10% of dietary iron is absorbed, in ferrous (2+) form and enters plasma in the ferric form, in duodenum and jejunum. Absorption is increased in pregnancy and iron deficiency states, controlled in epithelial cells. excess iron forms ferritin and is shed with cells in the gut lumen
Iron is bound to transferrin in the portal bloods and carried to the bone marrow where it is mainly used for Erythropoiesis. c.6g of haemoglobin are produced each day requiring c.20mg of iron. Total plasma turns over c.7x/day
Iron is storre bound to reffitin and haemosiderin
Ferritin
water soluble protein iron complex
composed of apoferritin and iron-phosphate-hydroxide core
20% of its weight is iron
synthesis is stimulated by the presence of iron
iron is in the ferric (3+) form
Haemosiderin
insolube protein-iron complex
40% of it’s weight = iron
formed by lysosomal digestion of ferritin
Transferrin
B-globulin synthesised in the liver
Iron Deficiency Anaemia
Commonest cause of anaemia worldwide
Hypochromic and microcytic red blood cells
Sx= lethargy, dyspnoea, skin atrophy, koilonychia, angular stomatitis, glossitis, oesophageal/pharyngeal webs
Causes:
- Increase loss - uterine, GI, urine
- Increased demands - prematurity, growth, child bearing
- Malabsorption - post gastrectomy, coeliac disease
- Poor diet
Investigation:
- FBC - Hb M<13.5, W<11.5, MCV <76, MCH <27, MCH conc <300
- Blood film - microcytic, hypochromic red cells
- other causes: anaemic of chronic disease, thalassaemia trait, sideroblastic anaemia
- haematinic assay (serum ferritin <10, iron M<14, W<11, vitamin B12, folate)
- Faecal occult blood
- Mid-stream urine
- Endoscopic or radiological studies of GI tract
Management:
- Oral replacement; ferrous sulphate, fumarate gluconate
- 200mg of iron/day
- SE: epigastric pain, constipation, diarrhoea
- aim: increase Hb conc 1g/L/dau. continue for 3 mo post normal Hb achievement
- IV iron - if oral not tolerated
- SE: anaphylaxis, skin staining, arthralgia
Sickle cell
AR - single amino acid substitution in B chain, Valine-> glutamic acid at position 6, Homozygous = Sickle cell disease, heterozygous = sickle cell trait, Hb S = less soluble than Hb A & when deoxygenated -> polymerisation -> sickle cells -> blockage of small vessels -> vaso-occlusive event. Sicking precipitated by infection, fever, dehydration, cold, hypoxia. Blood film = chronic haemolytic anaemia with high reticulocyte count, @risk of infection by encapsulated bacteria
Acute complications:
- Painful crisis
- 60% of pt have 1 episode/yr, bony crisis = localised ischaemia ?AVN, rest and analesia. Abdo crisis = abdo pain, vomiting, distension, features of peritonism. c.40% adolescence with SCD have gallstones
- worsening anaemia
- due to acute splenic sequestration/aplastic crisis PC: tiredness, cardiac failure, URGENT transfusion
- acute chest symptoms
- CP, cough, fever, tachypnoea XR=consolidation. Chlamydia/mycoplasma = important causes of chest infection. Mx = parenteral ABx
- symptoms and signs of neurological/ocular events
- stroke in c.10% of pt <20yrs, Acute stroke -> URGENT exchange transfusion
- priapism
- 20% before 20 yrs, if >few hrs-> impotence. Mx - blood aspirated from copura. Intra-cavernosal injection of alpha agonist e.g. phylepherine
Investigation/diagnostics:
- sickle solubility test
- high performance liquid chromatography
Patient should avoid cold, dehydration, take prophylacitc ABx (phenoxymethylpenicillin & vaccination with pneuomococcal vaccine), @risk of acute sicking complications with GA, pre/peri op Mx ?exchange transfusion, ensure adequate pain relief
Management of pt with suspected complications
- IVF
- adequate pain relief with optiates
- O2
- early ABx therapy is suspected infection
Haemostasis
- 3 elements:
- vasoconstriction
- vessel injury + vasoconstrictive elements from platelets + (pain ->) reflex sympathetic vasocontriction
- platelet aggregation
- platelets are formed in BM from megakaryocytes. Contain contractile proteins e.g. actin and myosin, no nucleus, endoplasmic reticulum and golgi apparatus -> proteins, mitochondria -> ATP/ADP. Synthesise prostaglandins and thromboxane A2. 1/2 life of 8-12 days. Tissue damage -> plts aggregation -> plt plug & adhere to damaged endothelium via von willebrand factor. Aggregating platelets release arachadonic acid which is converted to thromboxane A2. Ca mediate contraction of actin and myosin -> degranulation. Release of ADP -> further aggregation, positive feedback fashion
- clotting cascade
- 2x semi independent pathways; intrinsic (within bld, slow 2-6mins), extrinsic (fast 15secs, triggered by extravascular tissue damage, activated by exposure to tissue factor). Both pathways -> acivtation of prothrombin (Factor II) -common pathway-> fibrinogen converted to fibrin monomers which polymerise -> long fine strangds held together by H bonds later converted to covalent bonds with stabilisation of the fibrin polymer.
- vasoconstriction
Prothrombin time - PT
- Measure of extrinsic and common pathways
- add thromboplastin and calcium to the patients plasma
- PT is expressed as a ratio aka International Normalise Ratio.
- Prolonged in:
- Warfarin Treatment
- Liver disease
- Vit K deficiency
Activated partial thromboplastin time - APTT
- Tests intrinsic and common pathways
- Add Kaolin to pt plasma
- Prolonged in:
- Heparin treatment
- Haemophilia & factor deficiencies
- Liver disease
- Disseminated intravascular coagulation
- Massive transfusion
- Lupus anticoagulation
thrombin time
- Tests common pathway
- Thrombin is added to pt plasma
- converts fibrinogen into fibrin
- Prolonged in:
- heparin treatment
- DIC
- Dysfibrinogenaemia
Bleeding time
- measures capillary bleeding
- Prolonged in:
- Plt disorders
- vessel wall disorders
Bleeding diasthesis
- Vessel wall :
- Hereditary haemorrhagic telangiectasia
- Ehlers-Danlos syndrome
- Drugs e.g. steroids
- Sepsis
- Trauma
- Vasculitis
- Platelets
- Congenital plt disorders
- Thrombocytopenia
- Myeloproliferative disorders
- Drugs e.g. aspirin
- Coagulation system
- von Willebran’s disease
- Factor VII, IX deficiency (haemophilia)
- Liver disease
- Anticoagulants
- DIC
Haemophilia
- Haemophilia A = Factor VIII deficiency
- 1 in 10, 000 pop
- Haemophilia B = Christmas disease = Factor IX deficiency
- Sex linked disorder by c.1/3rd = no family Hx
- PC: childhood, prolonged haemorrage after dental extraction, recurrent haemarthroses/muscle haematomas, subperiosteal haemartomas -> haemophilic pseudo-tumours
- Severity correlated to clotting factor activity:
- <1% clotting factor activity -> severe disease with life-threatening bleeding
- 1-5% activity -> moderate disease with post traumatic bleeding
- 5-20% activity -> mild disease
- Ix: Prolonged APPT, Normal PT, BT prolonged, Factor VIII levels reduced
- Treatment:
- Factor VIII replacement either as F8 concentrate/cryoprecipirate
- bleeding is well controlled when FVIII levels >20%
- 5-10% pt develop antibodies to factor VIII and become refractory to replacement Rx
- Desmopressin -> increases intrinsic factor VIII levels
- Factor VIII replacement either as F8 concentrate/cryoprecipirate
von Willebrand’s disease
- Dysfunction/deficiency of vWF
- vWF -> mediates adhesion of plts to sites of vascular inj and bind & stabilises procoagulant protein factor VIII
- Haemostasis is imparied due to defective interaction between plts and vessel wall
- PC: skin bruising, node bleeds, haematoma, prolonged bleeding from trivial wounds
- Dx; demonstrate a deficiency of vWF
- Rx: desmopressing
Recombinant factor VIIa
- VIIa = Trypsin like serine protease = initiator of thrombin generation
- via 2 pathways -> activates factor Xa
- at site of tissue injury complexed with tissue factor
- TF found in subendothelial layer of vascular wall, not normally available to complex with factor VIIa but exposed following vessel wall injury
- on platelet surface independent of tissue factor
- at site of tissue injury complexed with tissue factor
- via 2 pathways -> activates factor Xa
- Recombinant VIIa - licensed for use in haemophiliacs with Abs to Factor VIII
Disseminated intravscular dissemindation
- widespread intravascular activation of the clotting cascade -> consumption of blotting factors -> bleeding tendency
- PC: bruising, purpura, oozing from surgical wounds/venepuncture
- Causes:
- Severe (usually gram neg/meningococcal) infection
- Widespread mucin-secreting metastatic adenocarcinoma
- Hypovolaemic shock
- Burns
- Transfusion reactions
- Eclampsia
- Amniotic fluid embolus
- Promyelocytic leukaemia
- Investigations:
- APPT andPT increased
- Serum fibrinogen levels reduced
- Fibrin degredation products increased
- Thrombocytopenia
- Factor V and VIII activities reduced
- Management:
- Fluid resuscitation
- Rx cause
- Clotting abnormalities corrected with FFP, cryoprecipitate and plt transfusion
Blood transfusion; blood products
- Whole blood
- Packed red cells
- Granulocyte concentrated
- Plt concentrates
- Human plasma - FFP
- Plasma protein fraction
- Human albumin 25%
- Cryoprecipirate
- Clotting factors VIII/IX
- Immunoglobulins
Blood groups…
- ABO system:
- 3 allelic genes - ABO
- A and B genes control synthesis of enz that add carbohydrate residues to cell surfact glycoproteins
- O = amorph and does not transform glycoprotein
- 6 possible genotypes + 4 phenotypres
- Naturally occurring ABx are found in serum of those lacking corresponding Ag
- O = universtal donor
- AB = universal recipient
- 3 allelic genes - ABO
- Rhesus:
- immune antibodies requiring prior exposure during transfusion/pregnancy
- 85% of pop are +ve, 90% are -ve
- negative pt transfused with rehesus +ve blood -> anti D antibodies
- Cross match = 3 stages
- 1 - blood grouping - pt red cells are grouped for ABO and Rhesus antigens
- Serum test is performed to confirm ABO group
- 2 - antibody screening to detect atypical red cell antibodies in recipient’s serum
- 3 - cross match to test donor red cells (antigens) against pt’s serum (antibodies)
- 1 - blood grouping - pt red cells are grouped for ABO and Rhesus antigens
Complications of blood transfusion
- Early:
- Haemolytic reactions (immediate/delayed)
- BActerial infections from contamination
- Allergic reactions to WC/platelets
- Acute lung injury
- Pyogenic reactions
- Circulatory overload
- Air embolism
- Thrombophlebitis
- Citrate toxicity
- Hyperkalaemia
- Clotting abnormalisties
- Late:
- Infections - hepatitis/CMV
- Iron overload
- Immune sensitisation
Acute haemolytic (incompatible blood)/ bacterial (infected blood) transfusion reactions:
- Difficult to differentiate on clinical grounds
- High morbidity/mortality
- In unconscious pt - DIC may be the only indicator
- ABO mismatch - normally due to human error
- Pt = unwell/agitated
- Sx: back pain, pain @ site of infusion , SOB, rigors
- Ex: hypotension, oligouria, bleeding from enepuncture sites
- Urinalysis = haemoglobinuria
- Bld tests - FBC, plasma haemoglobin, clotting, blood cultures, repeat grouping
- Mx: stop transfusion, remove giving set, IC crystalloid, broad spec ABx, monitor urine output
Anaphylaxis
- IgA deficiencies due to reaction to pt’s IgA
- PC: circulatory collapse, bronchospasm
- Transfusion discontinued, giving set removed, airway maintained and O2 given + adrenaline/chlorpheniramine/salbutamol
- Non-haemolytic transfusion febrile reaction
- @c.30mins
- PC: ‘well in self’, temp c.<38.5, bld pressure normal
- Mx: stop transfusion, consider more sig reaction, transfusion restarted at slower rate + paracetamol
Transfusion Related Acute lung injury
- followig administration fo plasma containing blood components
- Interaction of donor antibodies with recipient WVV
- Clinical picture = Acute Respiratory Distress Syndrome (ARDS) = fever, cough, SOB + CXR; perihilar shadowing
- @c.30mins-several days post transfusion
Delayed haemolytic transfusion reaction
- 5-10days after transfusion
- consider if - unexplained pyrexia, jaundice, drop in Hb
- Urinalysis = urobilinogenuria
Autologous transfusion
- pt own blood
- elective surgery
- reduces the need for allogenic blood transfusion and ind risk of post op complications e.g. infection, tumour recurrence
- 3 techniques:
- predeposit transfusion
- Blood collection c.2-5wks preop, 2-4 units storred, eliminates risk of viral transmission and reduces the risk of immunological transfuion reactions, reduces the need of post op immunosuppression seen with allogenic transfusion. Collection = expensive and time consuming
- Intra-op acute normovolaemia haemodilution
- whole blood removed at start of procedure and replaced with crystalloid/collloid, blood stored at room temp, re-infused during/immediately post op, cheaper than pre-deposit, little risk fof admin/clerical error
- Intra-op cell salvage
- shed blood is collected from op field, anticoagulated with citrate/heparin, filtered, washes with saline, concentrated by centrifugation and reindused
- CONTRAINDICATED in contaminated fields/presence of malignancy
- predeposit transfusion
Preop anaemia
Tissue oxygenation is dependent on arterial O2 content, cap blood flow, position on O2 dissociation curve, Hb conc affects all of these, anaemia reduces arterial O2 content, reduced plasma viscocity increased cap blood flow, increased 2,3 bisphosphoglycerate shift O2 dissociation curve to the right
Anaemia and polycythaemia increases post op mortality
Periop Hb conc of c.10g/dL is idea
Preop transfusion may induce immunospuppression , increase risk of infection, increase risk of tumour recurrence
give transfusion c.2 days preop
Autonomic Nervous System
- Sympathetic:
- Eyes - iris dilates
- Heart - HR increased
- Bronchioles - dilate
- Bladder - sphincter contricts, detrusor relaxes
- Intestine - secretions decrease
- Rectum - sphincter relaxes, muscle wall contracts
- Parasympathetic
- Eyes - iris constricts
- Heart - HR decreases
- Bronchioles - constrict
- Bladder -sphincter dilates, muscle wall constricts
- Intestine - secretions increases, motility increases
- Rectum - sphincter constricts, muscle wall relaxes
Sympathetic nervous system
- Thoracic and lumbar regions
- Preganglionic N (short) –Acetylcholine-> ganglia (paralel to spine cord)–noradrenaline->target
- e.g. adrenal medulla (endocrine gland) = combined autonomic ganglion and postsynaptic sympathetic nerve
- releases adrenaline and noradrenaline
- increase cardiac output, pulmonary ventilation, diverts blood to muscles, raises BM, slows digestion, slows kidney filtration
Parasympathetic nervous system
- Arises from cranial and sacral regions of the CNS
- CN incl III, VII, IX, X
- Long preganglionic nerve with synapse at ganglia near or on the organs innervated
- Acetylcholine is the neurotransmitter release from pre and post ganglionic neurones
- PSN = rest and digest, increases secretions, mobility of different parts of digestive tract, involved in urination and defecation
Adrenergic receptors
- Adrenergic = stim by noradrenaline and adrenaline
- Alpha 1
- smooth muscle of arterioles and sphincter muscles of GIT and Bladder
- Alpha 2
- presynaptic nerves and other parts of GIT
- Beta 1
- dominant type in <3
- Beta 2
- bronchioles of lung and muscles of bladder
Parasympathetic receptors
- nicotinic
- autonomic ganglia
- (different to those in neuromuscular junctions)
- muscarinic receptors
- organs with parasympathetic innervation
- acetylecholine = neurostimulator
Define pain
- pain is an unpleasant sensory and emotional experience asociated with potential or actual tissue damage
- Complex interaction of sensory, emotional and behavioural factors
- Stimuli activate nociceptive system which then conveys the information to the brain by an adaptable pathways
- Pain is only experiences in the conscious brain
Somatic Pain
-
First pain
- protective response which allows rapid withdrawal from painful stimulus due to stimulation of high threshold thermo/mechanical receptors
- Info transmitted by fast myselinated A fibres
- Enter the dorsal horn of the spinal cord
- Secondary fibres in spinothalamic tract transmit the stimulus to the posterior thalamic nuclei
- Tertiary fibres transmit the stimuli to somatosensory post-central gyrus
-
Secondary pain aka slow pain
- is responsible for the delayed sensation of pain
- Elicits behaviour to protect damaged tissue
- Initiates reflex responses e.g. Tachycardia, hypertension, increased RR
- Due to stimulation of high threshold polymodal receptors
- Responds to mechanical, thermal, chemical stimuli
- Info is transmitted by slow unmyelinated C fibres which enter the dorsal horn
- secondary fibres in palaeo-spinothalamic tract transmit the stimuli to the medial thalamic nuclei
- Collateral fibres transmit the stimulus to the midbrain, medullary reticular formation and hypothalamus
- Further info is transmitted to the forebrain limbic system
- Secondary fibres
Visceral pain
- fewer visceral nociceptor than somatic receptors and cortical mapping is less concentrated -> poorly localised pain
- qualitatively different due to progressive stimulation and summation
- referred to a site away from the source of stimulation
Physiology of nociception
Peripheral activation
- pain originates following tissue damage
- local release of inflammatory mediators incl:
- leukotrienes D4, B4
- Bradykinin
- Histamine
- 5HT
Acitvate or sensitive high threshold nociceptors and results in primary hydrealgesia
Spinal level activation
- occurs in dorsal horn of spinal cord
- Complex interaction between excitatory and inhibitory interneurones
- incl descending inhibitory tracts
- Gate control theory - explains non-linear relationship between inj and response
- pain can be gated out in the dorsal horn by other stimuli
- neurotransmitters = excitatory amino acids and neuropeptides
- increase nociception:
- substane P, bombesin, VIP
- Reduce nociception:
- galanin, somatostatin, GABA
- increase nociception:
Supraspinal level activation
- perception of pain assoc with acivity in the thalamus and primary & secondary cortex
- Various regions of the brain are involved with descending inhibition
- Stimuli originate at level of cortex and thalamus and are mediated via reflexes in brainstem and dorsal columns to the dorsal horns
- mediators involved incl: noradrenaline, 5HT, endogenous opioids
Adverse effects of post op pain
- Respiratory - reducced cough, atelectasis, sutum retention, hypoxaemia
- CV - increased myocardial O2 consumption and ischaemia
- GI - decreased gastric emptying, reduced gut motlity and constipation
- GU - urinary retention
- Neuroendocrine - hyperglycaemia, protein catabolism, sodium retention
- MSK - reduced mobility, pressure sores, increased risk of VTE
- Psychological - anxiety, fatigue
Management of pain
- Non-pharm:
- Pre-op explanation and education
- relaxation therapy
- Hypnosis
- Cold/heat
- Splinting of wounds
- Transcutaneous Electrical Nerve Simulation
- Pharm:
- simple analgesia
- Non-steroidal anti-inflammatory agents
- Opiates
- Local anaesthetic agents
Paracetamol
weak anti-inflammatory
Modulates prostaglanding production in the CNS
Orally/IV/Rectally
OD -> hepatic necrosis
NSAIDS
Inhibit cyclo-oxygenase enzyme
Reduce prostaglandin, prostacyclin, thromboxane
Weak central analgesic effect
‘opiate sparing’
SE: Gastric irritation, peptic ulceration, precipiration of bronchospasm in asthmatics, impairment of renal function, platelet dysfunction, bleeding
Opiates
- Diamorphine:
- prodrug rapidly hydrolysed to morphine and 6-monoacetyl-morphine
- Lipid soluble compared to morphine with greater central effects
- u receptors in the brain and spinal cord
- u1 = analgesic, u2 = resp depression
- SE: sedation, nausea, vomiting, vasodilatation, myocradial depression, pruritus, delayed gastric emptying, constipation, urinary retention
- Morphine
- IM, SV, IV (PCA)
- Lipid solube e.g. fentanyl - spinal/epidural
- Good analgesia, reduced SE
- Intrathecal morphine - targets CNS
Opiates - morphine
*
Local anaesthetic agents
Reduce membrane permeability to sodium
Act on small unmyelinated C fibres before large A fibres
Reduce pain and temp sensation before touch and power
- Lignocaine/lidocaine
- weak base, @physiological pH = ionised, rapid onset but short duration of action
- add adrenaline -> increase duration of action by c.2 hrs
- Plain lignocaine = local anaesthesia to digets/appendages due to risk of tissue ischaemia
- Main toxicity on CNS & CVS
- Bupivacaine
- chemically related to lignocaine, prolonged onset and longer duration of action
- acts for 6-8hrs
- Adrenatline can prolong action
- Main toxicity on CNS & CVS
Complications of spinal and epidural anaesthetic
- Spinal:
- Immediate:
- Hypotension - common
- local anaesthetic toxicity - rare
- High blockage - oaccational
- Early:
- Urinary retention - common
- Headache - 1-5%
- Local infection - almost never
- Meningism - uncommon
- Epidural haematoma - almost never
- Backache - common
- Immediate:
- Epidural :
- immediate:
- hypotension - less common
- Local anaesthetic toxicity - occasional
- High blockade - occasional
- Early:
- urinary retention - less common
- Headache - never unless dural puncture
- Local infection - uncommon
- Meningism - very rare
- Epidural haematoma - very rare
- Backache - common
- immediate:
Spinal and epidural anaesthesia
Spinal - LA/Opiate into CSF below termination of the spinal cord at L1
Epidural = LA/Opiate into fatty epidural space. Singl bolus -> good effect for several hours.
Quality often better with spinal
CI: pre-existing neurological disease, known coagulopathy, sepsis
Post op epidural infusion
attenutates post op stress response, improves post op pain control, reduces post op pulmonary comp, rapid return of GI function, as part of ‘enhanced recovery’ can reduce length of stay
Opioid alone -> analgesia without sedation, no motor or sympathetic blockage, SE: itch/resp depression after stopping infusion
LA alone -> anaesthesia with no sedative effect/resp depression, sympathetic and motor blockade = common. SE: CV, patchy/unilateral block.
Combination -> synergy = BEST!
Complications of epidural infusions
- Hypotension:
- sympathetic outflow T1-L2 = blocked with spinal/epidurals
- higher block = greater degree of sympathetic block
- hypovolaemic pt = higher risk of hypotension
- Rx = fluid resusc
- Post spinal headache:
- c.2%
- due to CSF leak
- settles c.3 days
- Chr = occipital, worse on standing, relieved by lying down
- Rx = bed rest, simple analgesia, fluids +/- blood patch (pt own blood injected into epidural space to seal the leak)
Postoperative Nausea and Vomiting (PONV)
- most unpleasant memoray assoc with pt surgical experience
- c.25% incidence
- Prolonged vomiting => electrolyte imbalance, dehydration, prolonged hospital stay
- Physiolgy, N&V = controlled by vomiting centre
- Efferent impulses influence other brainstem nuclei incl chemoreceptor trigger zone (CTZ) in the area postrema of the 4th ventricle outside the BBB
- Afferent stimuli from chemoreceptors and pressure receptors in gut + CNS and peripheral pain receptors + Other input from: cerebral cortex, vestibular, cerebellar nuclei
- dorso-lateral reticular formation of medulla (brainstem)
- Dopamine & 5HT -> important role in activity of CTZ
- 5HT = role in drug induced emesis e.g. 5HT3 receptors = role in N&V induced by cytotoxic agents
- acetylcholine & dopamine also play a role
Examples of anti-emetics
Domperidone, cyclizine, hyoscine, ondansetron
combination = increased efficacy
Fluid and electrolyte management
- ‘average’ man = 70Kg
- Body water = 60% of weight = 42 Litres
- Intracellular = 28L
- Extracellular = 14L
- EC = Plasma volume (3L) + extravascular volume (11L)
- Total body sodium 4200 mmol, 50% extracellular
- Total body potassium 3500 mmol, 50 mmol extracellular
- Osmolality of EC fluid = 280-295 mosmol/kg
Maintenance requirements
70Kg male = 3 L of water, 120 mmol Na, 70 mmol K
Child:
- 0-10 Kg = 100 mL/Kg
- 10-20Kg 1000mL + 50mL/kg
- 20+ = 1500mL + 25mL/kg
Pre-existing and on-going losses
- Often rich in sodium:
- Vomiting & diarrhoea
- Nasogastric aspirate
- Stoma, drain, fistula output
Insensible losses
- Faeces = 100mL/day
- Lungs = 400 mL/day
- Skin = 600 mL/day
- Total = c.1L/day
Composition of crystalloid solutions
Note requirements 70Kg man = 1L, 120mmol Na + 70 mmol K
- Hartmann’s:
- Na 131 mmol/L
- Chloride 111 mmol/L
- Potassium 5 mmol/L
- Bicarbonate 29 mmol/L
- Calcium 2 mmol/L
- 0.9% Saline:
- Na 150 mmol/L
- Cl 150 mmol/L
Fluid resuscitation
- Clinical assessment and obs used to guide resusc
- Dehydration:
- Tachycardia, hypotension, reduced skin turgor
- Urine output = degree of hypovolaemia = Oliguria = 0.5 mL/kg/Hr
- Fluid challenge = 200-250mL bolus, response:
- rapid rise and prompt fall = hypovolaemia
- Rise that is maintained = good intravascular volume replacement
Central Venous Access
- internal jugula - more often, R>L (pleura rises higher on left and thoracic duct on left), pt head down, triangle formed by 2 heads of SCM & clavicl, cannula aimed down and lateral towards ipsilateral inline nipple
- Subclavain vein - pt head down, approach below the clavicle, needle inserted below junction of medial 2/3 and lat 1/3 clavicle, needle towards suprasternal notch, pass immediately behind the clavicle, vein encountered @4-5cm
- Techniques:
- Seldinger
- Surgical cut down
- Catheter over needle
- Catheter through needle
Central venous access
Seldinger technique
- Technique:
- venepuncture with introducer needle
- soft tipped guide wire through needle, needle removed
- dilator over guide wire, dilator removed
- catheter over guide wire, guide wire removed
- Complications:
- Early:
- Haemorrhage
- air embolus
- pneumonthorax
- cardiac arrhythmias
- pericardial tamponade
- failed cannulation
- Late:
- Venous thrombosis
- Infection
- c.10% central lines become colonised with bacteria
- c.2% pt in ICU develop catheter related sepsis
- usually coagulase neg staph
- occassionally candida, staph aureus
- aseptic technique + line care + closed systems +-/- antimicrobial coating of line
- Early:
Central venous access
Surgical cut down
- Useful in shocked, hypovolaemic pt
- long saphenous @ ankle c.2cm ant to medial malleolus
- basilic vein at the elbow c.2.5cm lat to medial epicondyle
- Vein is dissected and ligated distally, small transverse venotomy is made, cannula passed through venotomy and secured
Surgical nutrition - sequelae of poor nutrition
- delayed wound healing
- reduced ventilatory capacity
- reduced immunity
- increased risk of infection
Assessment of nutrition
10% WL = mild
30% WL = severe
Anthropometric = triceps skin fold thickness, mid-arm circumference, hand grip strength
Methods of nutritional support
- Enteral:
- prevents intestinal mucosal atrophy
- supports gut associated immunological shield
- attenuates hypermetabolic response to injury and surgery
- cheaper than PN and fewer complications
- Polymeric liquid diet - short peptides, medium chain triglycerides, polysaccharides, vitamins, trace elements
- Route:
- short term: Orally/Via NG tube
- Longer term: surgical/percutaneous gastrostomy, jejunostomy
- Parenteral:
- intestinal failure - reduction in functioning gut mass to below the minimus necessary for adequate digrestion and basorption of nutrients
- Indications for PN:
- enterocutarnous fistulae
- moderate/severe malnutrition
- abdominal sepsis
- prolonged ileus
- major trauma and burns
- sever inflammator bowel disease
- PN: hyperosmolar, low PH, irritant to vessel walls. In 2.5L:
- 14g nitrogen as L amino acids, 250g glucose, 500mL 20% lipid emulsion, 100 mmol Na, 100 mmol K+, 150 mmol Chloride, 15 mmol Mg, 13 mmol Ca, 30 mmol phosphage, 0.4 mmol zinc, water and fat soluble vitamins, trace elements
- Monitoring PN:
- clinically -weight
- biochem 2x/wk:
- FBC, U&E, LFT
- Mg, Ca, zinc, phosphate
- Nitrogen balance
- Blood cultures/sign of spesis
- Metabolic complications of PN:
- hyponatraemia
- hypokalaemia
- hyperchloraemia
- trace element and folate deficiency
- deranged LFTs
- Linoleic acid deficiency
Post op complications - in accordance to timings
- <24hrs:
- systemic response trauma
- pre-existin infection
- 24-72 hrs
- pulmonary atelectasia
- chest infection
- 3-7 days
- chest infection
- wound infection
- intraperitoneal sepsis
- urinary tract infection
- anastomotic leak
- 7-10 days:
- DVT
- PE
Wound dehiscence
- Features
- c.2% of midline laparotomy wounds
- serious complication with mortality of up to 30$
- Failure of wound closure technique e.g. broken suture, slipped knot, inadequate muscle bites, presence of infection
- @c.7-10days post op
- heralded by serosanguinous discharge from wound
- even if clinically appears partial likely to effect the whole wound
- Management:
- Opiate analgesia, sterile dressing, fluid resus
- early return to theatre for resuturing under GA
- interupted sutures or mass closure with non-absorbable sutures
- deep tension sutures - controversial due to possible strangulation and muscle weakening
- Painful and assoc with increased risk of infection
Post op hypoxia
- lack of alveolar ventilation:
- hypoventilation (airway obstruction, opiates)
- bronchospasm
- pneumothorax
- arteriovenous shunting (collapse, atelectasis)
- Poor alveolar perfusion:
- ventilation- perfusion mismatch (PE)
- Impaired cardiac output
- decreased alveolar diffusion
- pneumonia
- pulmonary odema
Atelectasis
- first 48hrs post op
- due to reduction in functional residual capacity
- increease in volume of bronchial secretions, increase in viscocity of secretions, reduction in tidal volume and ability to cough
- Risk of sig atelectasis increases with:
- pre-existing lung disease
- upper rather than lower abdo incisions
- obese patients
- cigarette smokers
- Clinically:
- post op pyrexia @c.48hrs post op, accompanied by tachycardia and tachypnoea
- reduced AE, dullness on percussion, reduced breath sounds
- CXR - consolidation and collapse
- Treatment:
- intensive chest physio, nebulised bronchodilators, approp ABx for possible associated infection
Post op pneumonia
- nosocomial pneumonia = c.1% of all pt admitted to hospital in 15-20% of non-ventilated and 40-60% of ventilated ITU pt
- Organisms incl:
- gram neg bacteria (pseudomona aeruginosa, enterobacter)
- Staph aureus
- anaerobes
- haemophilus influenzae
- Aspiration pneumonia
- Chemical pneumonitis due to gastric contents
- apical segment of right lower lobe
- Secondary pacterial infection - gram negative and anaerobic organisms
- Treatment: tilting head of op table down and sucking out the pharynx
- Prophylactic ABx
- Chemical pneumonitis due to gastric contents
Post op CV complications
- Hypotension
- hypovolaemia
- ventricular failure
- cardiogenic shock
- arrhythmias, due to:
- physiological disturbances - acidosis, hypercapnoea, hypoxaemia
- electrolyte imbalances
- vagal manoeuvres
- hypovolaemia
- pathological disturbances - myocardial ischaemia, pulmonary embolus
- pharmacological agents
- conduction defects
- Hypertension
Post op renal failure - causes
- Causes:
- pre-renal
- shock (hypovolaemia, cardiogenic, spetic)
- renal artery disease
- renal
- acute tubular necrosis
- glomerulonephritis
- intestinal nephritis
- post-renal
- bladder outflow obstruction
- single ureter (calculus, tumour)
- both ureters (bladder malignancy)
- pre-renal
Urinary infection
- 10% of pt admitted to hospital have a catheter inserted
- Bactera colinisation of catheters is common
- If catheter is required for >2wks, 90% of pt -> bacteriuria
- commenect ogranisms = enterobracter, enterococci
- colonisation DOES NOT require teatment
- Infection = prevented by maintining a closed drainage system, good infection control standards, preventing backflow of urine from catheter bag
Post op confusion
- assoc with increased morbidity and mortality, and length of stay
- Clinical features: reduced level of consciouness, impaired thinking, memory and perceptional abnormalities, disturvance of emotion
- Causes:
- Pain (and unable to sleep or move around)
- Infection - intra/extracranial
- Nutrition
- Neoplasia - primary, secondary brain tumours
- Constipation (or unable to pass urine properly)
- Hydration (dehydration and malnutrition - thiamine wernicke’s encephaolpathy, B12 def)
- Hypoxia - resp disease, CF, arrhythmia
- Electrolytes
- Endocrine - hypothyroid, hypethyroidism, addison’s
- Stroke - CVA/TIA + head injury
- Medication (sudden stopping or starting drugs, alcohol)
- Environment (being in an unfamiliar place)
Early warning scores
- Heart Rate
- Blood Pressure
- Respiratory Rate
- Temperature
- Conciousness level
Low score - increas freq of obs
Medium score - request medical review
High score - request critical care assessment
Criteria for critical care assessment
- Threatened airway
- Respiratory arrest
- Resp rate >40 or <8
- O2 saturation <90% on >50% O2
- Cardiac arrest
- pulse rate <40, >140 bpm
- SBP <90
- Sudden fall in consciousness
- repeated/prolonged seizures
- rising arterial CO2 with resp acidosis
Criteria for critical care admission
Need for organ support
- Respiratory - ventilation/CPAP
- Renal - haemofiltration/haemodyalisis
- Cardiac - inotropic drugs
- Hepatic - blood transfusion
- Neurological - intracranial pressure monitoring
Factors to be considered when assessing admission to ICU:
- Diagnosis
- severity of illness
- age
- coexisting disease
- physiological reserve
- prognosis
- availability of suitable treatment
- response of treatment to date
- recent cardiopulmonary arrest
- anticipated quality of life
- patient’s wishes
Systemic inflammatory response syndrome - causes
- Sepsis - bacterial, viral, fungal
- hypovolaemic shock
- trauma
- burns
- tissue ischaemia
- pancreatitis
Definition of bacteraemia
presence of viable bacteria in the bloodstream
Definition of SIRS
Systemic inflammatory response to a variety of clinical insults manifested by 2 or more of the following:
- Temperatures >38, <36
- HR >90
- RR >20, PaCO2 >4.3
- WCC >12 or <4
Definition of sepsis
SIRS with documented infection
Severe SIRS
SIRS with documented infection and hypoperfusion, hypotension and organ dysfunction
Septic shock
sepsis with hypotension despite adequate fluid resuscitation
Pathophysiology of SIRS/Sepsis
failure to control inflammatory response
Over production of inflammatory mediators & under production of anti-inflammatory mediators, receptor abnormalities => initiation/propagation of response
decreased destruction of inflammatory mediators and production of abnormal leukocytes
SIRS/sepsis - Major inflammatory mediators
- Major inflammatory mediators:
- platelet activating factor
- tumor necrosis factor alpha
- Interleukin -1
- Interleukin-6
- Interleukin-8
- Interleukin-10
SIRS/sepsis - clinical features
- Obs:
- increased cardiac output
- decreased vascular resistance
- increased oxygen consumption
- Fever/hypothermia
- Tachycardia
- Tachypnoea
- Metabolic/haematological
- resp alkalosis
- deranged liver function
- derange renal function
- altered WCC & plts
- Disseminated Intravascular Coagulation
Severe sepsis = sepsis plus 1 of the following signs of hypoperfusion or organ dysfunction
- Areas of mottled skin
- CRT >/= 3 secs
- Urine output <0.5mL/Kg for at least 1 hr
- Lactate >2 mmol/L
- abrupt change in mental status
- abn electroencephalographic findings
- pl cnt <100,000 plt/mL
- DIC
- acute lung injury or acute respiratory distress syndrome
- cardiac dysfunction - echocardiography/cardiac index
Management of sepsis
prompt assessment and resusc#earky control the source of sepsis
Sepsis 6
- High flow O2
- Blood cultures
- IV ABx within 1 hr
- Fluid resuscitation
- VBG - Measurements of lactate and heamoglobin
- Catheterised and monitor urine output
Causes of unreliable pulse oximetry
- Intense vasoconstriction
- Jaundice
- Methaemoglobinaemia
Define respiratory failure
Inadequate gas exchange with the result that arterial oxygen and.or carbon dioxide levels cannot be maintained within their normal ranges
Type 1 (hypoxaemic) = reduced PaCO2 and reduced PaO2
Type 2 (ventilatory) = increased PaCO2 and reduced PaO2
=> Hypoxaemia and Hypercapnia
Causes of Type 1 Respiratory failure
Reduced PaCO2, Reduced PaO2
- Low inspired oxygen partial pressure
- alveolar hypoventilation
- Diffusion impairment
- ventilation to perfusion mismatch
- right-to-left shunt
Causes of type 2 Respiratory failure
Increased PaCO2, reduced PaO2
- Abnormalities of central respiratory drive
- neuromuscular dysfunction
- abnormalities of chest wall
- abnormalities of the airway
- abnormalities of the lung
Indications for tracheal intubation incl
- Facilitation of mechanical ventilation
- Protection from aspiration
- Facilitation of teacheobronchial suction
- Relief of upper airway obstruction
Indications for mechanical ventilation
- Support in resp failure
- coma (head injury/drug overdose)
- Control Intra-cranial Pressure
- Reduction of metabolic demands
- Allow muscle relaxation and facilitate surgery
- Post-operative ventilation
What are the different modes of ventilator support?
- Controlled mechanical ventilation
- assisted controlled or triggered ventilation
- Intermittent mandatory ventilation
- Pressure support
What are the variables that can be altered on a ventilator?
- Tidal volume
- ventilation rate
- insp to exp ratio
- flow waveform
- partial pressure of inspired O2
- preessure limit
- positive end exp pressure PEEP
- positive airway pressure CPAP
Complications of mechanical ventilation
- Problems associated with endotracheal tube - obstruction, misplacement
- disconnection
- barotrauma
- impaired venous return
- sodium and water retention
- bronchopneumonia
Pathology of ARDS
Diffuse alveolar damage
endothelial injury -> increased pereability
protein rich exudate in alveoli
neutrophils = important in inflammatory process
cytokines and enzymes - responsible for many of the features
resolution of inflammation cn occur but is usually associated with some degree of pulmonary fibrosis
Causes of ARDS
- Direct lung injury:
- pneumonia
- aspiration pneumonitis
- pulmonary contusion
- fat embolism
- inhalation injury
- Indirect lung injury:
- sepsis
- trauma
- cardiopulmonary bypass
- acute pancreatitis
Diagnosis and management of ARDS
PC: acute resp failure, hypoxaemia refractory to increasing resp support.
Dx: bilateral pulmonary infiltrates on chest XR, pulmonary capillary wedge pressure <18mmHg, no evidence of left atrial hypertension
Mx: supportive intensive care therapy, Rx cause e.g. ABx for sepsis, careful fluid balance, nutritional status addressed, mechanical ventilation
Acid-Base balance
Biological buffering mechanism to maintain pH 7.35-7.45, involving proteins, bicarbonate, haemoglobin
Relationship between serum pH and bicarb = henderson-Hasselbach equation
- Look at pH - acid <7.35, alkalosis >7.45
- Assess resp component, high CO2 -> Acidotic
- Assess metabolic component, high HCO3 -> Alkalotic
- Calculate anion gap (i.e. metabolic acidosis with/without an elevated anion gap)
Shock
pathological condition characterised by inadequate tissue perfusion reducing the delivery of oxygen and other essential nutrients to a level below that required for normal cellular activity
Cellular injury and destruction may follow and tissue & organ function deteriorate
Progressive CV collapse resulting in:
- Hypotension
- hyperventilation
- reduced level of consciousness
- Oliguris
Causes of shock include:
- Hypovolaemia
- cardiogenic
- septic shock
- anaphylaxis
Acute blood loss
Hb and PCV remain normal for first 3-4hrs
Plasma volume expands and Hb and PCV then fall
(assoc with increased neutrophils and plts)
Reticulocyte cnt increases day 2/3 -> maximum of 10-15% by day 8/10
without treatment Hb starts to rise by day 7
Acute Renal Failure
reduction in excretory or regulatory function resulting in the retention of waste products normally excreted by the kidney
Normal adult, urine output = 0.5ml.Kg/Hr
Renal failure = anuric, oliguric, polyuric
Biochem changes of ARF: Hyponatraemia, hyperkalaemia, hypocalcaemia, metabolic acidosis
Management: Rx cause (often fluid resuscitate/inotropes) + O2
Treatment of hyperkalaemia
10mL 10% calcium gluconate IV
10 units actrapid 50mL 50% dextrose
Salbutamol neb
Calcium resonium 15-30mg as required up to 2x/day
APACHE II Score
general measure of disease severity based on current physiological measurements, age, previous health condtions, 0-81
Increasing score = increasing change of hospital death
- made up of:
- acute physciology score
- age points
- chronic health problems
