Bronchial Asthma

Anesthetic Management of Pt. with Bronchial Asthma

Definition:

➧ It is an acute obstructive pulmonary disease. It is due to hyperreactivity of the tracheobronchial tree, in which some exogenous or endogenous stimuli can produce reversible airway obstruction.

➧ Histamine and the leukotrienes are the most active chemical mediators, while acetylcholine contributes via a disturbance in autonomic balance by stimulation of M3 cholinergic receptors on bronchial smooth muscles causing bronchospasm.

Pathological changes: (Figure 1)

-Prolonged expiration

-Increased residual volume and functional residual capacity

-Increased work on breathing

-Reduced vital capacity, inspiratory capacity, and expiratory reserve volume

-Ventilation-perfusion inequalities

-Hypoxia

-Bronchospasm

-Mucus secretion

-Edema of the bronchial mucosa

-Epithelial desquamation

Figure 1: Pathological changes in Br. Asthma 

Anesthetic Management:

Preoperative:

a) Assessment:

1-History:

-Wheezing, dyspnea, cough, and sputum production.

2-Classification of Asthma:

-Mild Intermittent: Mild symptoms up to two days a week and up to two nights a month

-Mild Persistent: Symptoms more than twice a week, but no more than once in a single day

-Moderate Persistent: Symptoms once a day and more than one night a week

-Severe Persistent: Symptoms throughout the day on most days and frequently at night

3-Drug Therapy:

-β2-adrenoceptor agonists (albuterol, levalbuterol, salbutamol, terbutaline, salmeterol, formoterol) 

-Xanthine derivatives (theophylline, aminophylline)

-Anticholinergics (Ipratropium bromide)

-Corticosteroids (beclometasone, budesonide, fluticasone, flunisolide, ciclesonide, mometasone).

-Mast cell stabilizers (sodium cromoglycate, nedocromil sodium)

-Leukotriene modifiers (montelukast, pranlukast, zafirlukast, zileuton)

-Allergy medications (allergy shots (immunotherapy), omalizumab)

4-Examination:

-Pulsus paradoxus

-Chest auscultation: The chest may be hyper resonant, with diminished breath sounds, prolonged expiration, and audible wheezes. In very severe cases the wheezes disappear

5-Investigations:

1. CBC:

-Polycythemia (if there is chronic hypoxemia)

-Eosinophilia: indicates the degree of airway inflammation

-Neutrophilia: bacterial infection

-Lymphocytosis: viral infection

2. Chest X-ray (CXR):

-Baseline for postoperative follow up

-May show an increase in bronchovascular markings and hyperinflation

-In the later stages, may show some degree of emphysema

-In an acute asthma attack, a CXR is essential to exclude pneumothorax

3. Arterial Blood Gases (ABG):

-Hypoxemia, Hypercarbia

4. Pulmonary Function Tests (PFT):

a) Tests indicate Severe Obstruction:

-Peak Expiratory Flow Rate (PEFR) of less than 120 l/min.

-Maximum Voluntary Ventilation (MVV) of less than 50% of predicted

b) Tests indicate the need for Postoperative Mechanical Ventilation (MV):

-FEV1 of less than 1 liter

-FEV1/VC ratio of less than 40% of predicted

-Increased PaCO₂ > 50 mmHg

c) Assessment of Severity of Asthma by PFT:

-Mild, Moderate, Severe, Very severe (Status asthmaticus or Respiratory failure)

d) Prediction of Postoperative Elective MV:

-PaCO₂ > 50 mmHg, PaO₂ < 50 mmHg, PFT < 50% of predicted

6-Risk assessment:

-Respiratory risk index score: predict postoperative respiratory complications or failure

b) Preparation:

1-Elective surgery should not take place in the presence of infection or untreated bronchospasm

2-Continue treatment: (Bronchodilators, Corticosteroids, …) up to the time of surgery

3-Pulmonary function tests and blood gases can be improved after the administration of bronchodilators

4-Stop smoking

5-Treatment of respiratory tract infection: Antibiotics after culture and sensitivity tests

6-Wait 2-3 weeks after clinical recovery of URTI (due to increased airway reactivity)

7-Treatment of complications if present: Dysrhythmia, Pulmonary HTN, Cor-pulmonale, Congestive heart failure

8-Chest physiotherapy: to remove secretions

9-Incentive spirometry: to improve lung expansion

10-Weight reduction of obese patients prepared for elective surgery

11-In severe cases it is important to assess the need for postoperative mechanical ventilation and reserve an ICU bed

c) Premedication:

1-Sedation:

-Anxiety may be a significant feature in the asthmatic patient, but a sedative premedication, such as an antihistaminics or benzodiazepine, is advantageous.

2-Anticholinergic:

-Atropine (to decrease bronchial secretions and vagal tone) 1-Atropine may be desirable for a smooth induction. It has a drying effect on secretions and can also improve dilatation in the larger bronchi by blocking vagal constrictor effects.

3-Corticosteroid Cover: if steroids have been used within the previous 3 months.

4-Avoid H2 blockers: lead to unopposed H1 bronchoconstriction.

Intraoperative:

a) Monitoring:

-ECG, NIBP, Pulse Oximeter, Capnography

-Pulsus paradoxus is present with Severe asthma & Tension pneumothorax (drop-in SBP ≥ 10 mmHg during inspiration) (Figure 2)

-Ventilator waveforms: Flow-Time scalar

-Spirometry: Volume-Pressure & Flow-Volume loops

Figure 2: Pulsus Paradoxus 

b) Precautions:

1-Avoid:

-β-blockers

-Histamine releasing drugs (Thiopental, Succinylcholine, Atracurium, Morphine, Meperidine)

2-Drug interactions:

-Ketamine + Theophylline → Seizures

-Halothane + (Aminophylline, β2-agonists, Hypercapnia) → Dysrhythmia

c) Regional anesthesia:

1-Avoid block above T6 as it leads to decreased Expiratory Reserve volume and decreased use of accessory m. → Ineffective cough and Retention of secretions → Postoperative respiratory complications.

2-Regional a. may be used for surgery or during labor. Epidural anesthesia could be safely administered to asthmatic parturients, even during acute exacerbations of asthma.

d) General anesthesia:

Induction:

1-Preoxygenation

2-Smooth induction, Warm, Humidified gases.

3-Blunt reflex bronchospasm induced by intubation (increase depth of anesthesia, Lidocaine, β2-agonist inhaler).

4-The use of IV lidocaine (1-1.5 mg/kg) before induction has been recommended, as it can prevent reflex bronchospasm, but not that resulting from the release of allergic mediators. However, topical lidocaine spray is not effective and can induce bronchoconstriction in asthmatic patients.

5-Bronchoconstriction can arise from the drug itself, or directly from tracheal intubation. Even when attacks are infrequent, tracheal intubation is one of the commonest causes of intraoperative bronchospasm in patients who have any history of asthma. The carina is particularly sensitive to stimulation.

6-Use of a laryngeal mask airway (LMA) has been shown to avoid the reversible bronchoconstriction associated with tracheal intubation.

Induction agents:

-Avoid Thiopental as it causes histamine release.

-Propofol, Ketamine, Etomidate, Benzodiazepines: are suitable agents.

-Ketamine: is a suitable induction agent for emergency anesthesia in asthmatics when a rapid sequence induction is required, as it has a protective effect against bronchospasm through sympathomimetic action by inhibition of noradrenaline reuptake, which was abolished by beta-adrenoceptor blockers.

-Inhalational induction:

-With Halothane or Sevoflurane in pediatric patients.

-With Sevoflurane can be given for emergency cesarean section in a patient with status asthmaticus.

Neuromuscular blockers:

-Succinylcholine: causes histamine release.

-Atracurium: constricts peripheral airways in doses that produce significant cardiovascular effects, and this probably results from histamine release which acts on H2 receptors. The peak effects occur 3 min. after a dose of 0.5 mg/kg. 

-Cis-atracurium, Rocuronium, Vecuronium, and Pancuronium: are suitable agents.

Inhalational agents:

1-Avoid N₂O if there is large emphysematous bullae (rupture, tension pneumothorax) or pulmonary HTN (increased PVR → pulmonary edema).

2-Inhalational agents are potent bronchodilators, however, in severe asthma, they can worsen ventilation-perfusion inequalities and increase hypoxia, by reducing hypoxic pulmonary vasoconstriction.

3-Halothane can interact with Aminophylline to produce serious arrhythmias (ventricular fibrillation and ventricular tachycardia), even when theophylline levels are within the therapeutic range. Halothane also sensitizes the heart to the effect of exogenous and endogenous catecholamines.

4-Halothane, Isoflurane, and Enflurane are all effective at reversing antigen-induced bronchospasm. The effect of halothane is secondary to the blocking of baseline vagal tone.

5-The choice of Isoflurane, Sevoflurane, and Enflurane may therefore be more appropriate.

Controlled MV:

1-Use warmed, humidified gases

2-Parameters: VT: 10-15 ml/kg, RR: 6-10 b/min., decrease TI, increase TE, decrease inflating pressure

3-Avoid PEEP

Fluid management:

-Adequate hydration: (less viscid secretions)

Intraoperative Complications:

1-Bronchospasm: There is an increased sensitivity to airway manipulations during light anesthesia. Tracheal tube insertion can induce reversible bronchoconstriction (acute bronchospasm), triggered by mechanical stimuli, but not with an LMA.

Treatment of Acute Bronchospasm:

-Identify the cause

-If this occurs following tracheal intubation, the easiest initial maneuver is to deepen the anesthetic using a volatile agent or β2 agonist inhalation through the inspiratory limb of the breathing circuit or ETT adaptor (Figure 3)

Figure 3: Application of β2-agonist inhaler through ETT adaptor

-IV Salbutamol 5-15 µg/kg in 10 ml saline over 10 min., for continued problems, a salbutamol infusion, 1-5 µg/kg/min. (with ECG monitoring)

-IV Aminophylline 5-6 mg/kg over in saline over 20 min. then 0.5-1 mg/kg/h. (with ECG monitoring)

N.B.1: Reduce aminophylline infusion rate by 30% because GA decreases hepatic blood flow by 30% and consequently aminophylline metabolism

N.B.2: Aminophylline has a narrow therapeutic index so, plasma theophylline levels must be measured if treatment is prolonged for more than 24 h. The therapeutic range is 10-20 mg/l but toxic effects such as fits, arrhythmias, and cardiac arrest have been described with plasma levels as low as 25 mg/l. Extreme caution is necessary if the patient has already been taking sustained-release theophylline preparations

-IV Hydrocortisone 1-2 mg/kg

-IV Ketamine in subanesthetic dose (bolus dose 0.75 mg/kg, infusion of 0.15 mg/kg/h) has been used to treat intractable bronchospasm

-IV Epinephrine 1 in 10 000 should be given in divided doses, 1-10 ml if there is complete airway closure. This may need to be repeated

2-Air trapping (Auto-PEEP, Intrinsic PEEP): due to decreased expiratory time, increased airway pressure, congested neck veins, decreased pulse pressure, hypotension due to decreased venous return and consequently cardiac output

3-Cardiac Dysrhythmias: can occur more frequently in the presence of hypoxia, hypercarbia, and acidosis, or following the overuse of sympathomimetic agents

4-Complications due to Drug interactions: mentioned before

5-Sudden Death: has been attributed to the combination of nebulized high dose β2-sympathomimetics and long-acting theophylline derivatives

The reverse of Neuromuscular blockers:

-Anticholinergic (Atropine) first then Cholinesterase inhibitor (Neostigmine)

Extubation:

-Deep extubation

-Awake extubation: blunt reflexes with IV lidocaine (1-1.5 mg/kg) first

Postoperative:

1-Monitoring, Semi sitting, Humidified O₂

2-Analgesia: NSAIDs (with caution), Local or regional a., Avoid Opioids can cause respiratory depression

3-Continue preoperative treatment

4-Avoidance of MV in a severe asthmatic was achieved by administration of a subanesthetic dose of halothane in 100% oxygen using a close-fitting mask

5-Elective MV if predicted preoperative or if indicated postoperative

Indications for Postoperative MV in Asthmatic Patients:

1-Distress and exhaustion

2-Deterioration in ABG. PaO₂ < 6.7 kPa (50 mmHg) or PaCO₂ > 6.7 kPa (50 mmHg), and increasing metabolic acidosis

3-Cardiac dysrhythmias or hypotension

4-Acute crises such as cardiorespiratory arrest, decreased conscious level due to sedatives, or a collapsed lung

5-Refractory asthma has been treated in the ICU with Magnesium sulphate, Halothane, and Propofol

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Local Anesthetic Toxicity

Local Anesthetic Toxicity

Clinical Manifestations & Management: 

1-CNS manifestations: 

➧ Early signs: circumoral numbness (Earliest sign), tongue paresthesia, dizziness

➧ CNS Excitation: (restlessness and agitation)

➧ CNS Depression: (slurred speech, drowsiness, unconsciousness)

➧ Muscle twitching, tonic-clonic seizures

➧ Respiratory arrest often follows

Management: 

1-Stop LA injection or infusion 

2-Call for help 

3-Oxygenation 

4-Hyperventilation (to decrease cerebral blood flow) 

5-Anti-seizures: Benzodiazepines (diazepam 0.1-0.2 mg/kg), Thiopental (1-2 mg/kg) 

2-Respiratory manifestations: 

➧ Local anesthetics (LAs) depress hypoxic drive (ventilatory response to low PaO₂)

➧ Apnea can result from phrenic and intercostal nerve paralysis

Management: 

➧ Respiratory support

3-CVS manifestations: 

➧ In general, LAs depress myocardial automaticity (spontaneous phase IV depolarization) and reduce the refractory period causing: bradycardia, heart block (varying degrees), and hypotension which may lead to cardiac arrest. 

➧ The R (+) isomer of bupivacaine rapidly blocks cardiac sodium channels and dissociates slowly. 

➧ Major cardiovascular toxicity requires about 3× the concentration required to produce seizures. 

➧ Ropivacaine is 70% less likely to cause severe cardiac arrhythmias than bupivacaine. 

Management: 

1-ACLS protocols 

2-Vasopressors: Ephedrine, Norepinephrine, Epinephrine

3-Lipid emulsion infusion: 

➧ Use of Lipid Emulsion: 

-IV bolus of Intralipid 20% (1.5 ml/kg over 1 min) about 100 ml and start infusion of (0.25 ml/kg/min) 

-If adequate circulation has not been restored: Repeat the bolus dose twice at 5 min intervals and increase the infusion rate to (0.5 ml/kg/min)

-Continue infusion until an adequate circulation has been restored

-Measure LA & triglyceride levels

Patient-related factors to consider during large volume peripheral nerve block (PNB): 

1-Age: 

➧ Newborns have about half the adult concentration of α-acid glycoprotein (AAG) which binds free LAs. 

➧ Persons over 70 years show increased sensitivity to LAs and decreased clearance. 

Recommendation: Reduce LAs dose by 10-20%. 

2-Renal dysfunction: 

➧ There may be a change in clearance of LAs in uremic patients. 

➧ Uremic patients show a rapid rise in LAs plasma levels probably secondary to a hyperdynamic circulation, but uremic patients have increased AAG levels. 

Recommendation: Reduce LAs bolus and continuous dose by 10-20% in uremic patients. 

3-Hepatic dysfunction: 

➧ Clearance of LAs can be dramatically decreased but plasma concentrations remain close to normal secondary to increased volume of distribution (Vd). These patients also can have renal and cardiac dysfunction. 

Recommendation: Initial bolus dose can be in the normal dose range but the continuous infusion dose should be reduced by 10-50%. 

4-Heart Failure: 

➧ Decreased blood flow to the liver and kidneys can cause a decrease in clearance

Recommendation: Repeat or continuous dosing of LAs should be reduced by 10-20%

5-Pregnancy: 

➧ Progesterone may increase the sensitivity of nerve axons

➧ There is an enhanced risk of cardiotoxicity by bupivacaine and ropivacaine induced by progesterone. Increased cardiac output causes increased uptake of LAs

Recommendation: Avoid large volume PNB in 1st trimester and reduce doses in epidural and spinal anesthesia in pregnancy

6-Drug interaction: 

➧ Amide LAs are cleared by the liver cytochrome P450 enzymes

➧ Propanolol, Cimetidine and Itraconazole can decrease bupivacaine clearance by 30-35%

➧ Ciprofloxacin and Fluvoxamine decrease the clearance of ropivacaine

Recommendation: Single bolus dose is of little concern but continuous infusion should be altered (10-20% decrease)

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Accidental Total Spinal Anesthesia

Accidental Total Spinal Anesthesia

Definition:

➧ A syndrome of the central neurological blockade. 

➧ It occurs when a volume of local anesthetic (LA) solution, intended for epidural anesthesia, enters the subarachnoid space and ascends to the cervical region.

Causes: 

a) After a known dural tap: 

➧ Accidental total spinal analgesia may occur in association with the original epidural after a known dural tap. 

b) After a top-up dose: 

➧ Following a top-up dose, as a result of accidental puncture of the dura by the epidural catheter. 

➧ High spinal anesthesia has occurred after top-ups of epidural catheters. 

➧ This is unlikely to result from catheter migration but may happen as a result of accidental puncture of the dura by the epidural catheter. 

➧ If part of the catheter lies within the epidural space and part within the subarachnoid, with a slow injection of LA, the solution will emerge from the proximal holes, and with a rapid one from the more distal. 

Presentation: 

1-Unexpected rapid rise in the sensory level. 

2-Numbness or weakness in the upper extremities. 

3-There is severe hypotension and bradycardia secondary to blockade of the sympathetic outflow. Occasionally cardiac arrest occurs. 

4-Rapidly increasing paralysis involves the respiratory muscles, due to phrenic nerve paralysis, resulting in apnea and hypoxia. 

5-The pupils become dilated and consciousness is lost. 

6-Cardiovascular collapse usually takes place immediately after the injection, although delays of up to 45 min. have been reported. 

7-Deaths have occasionally been reported. 

Duration: 

➧ Apnea may vary from 20 min. to 6 h, unconsciousness from 25 min. to 4 h, while full recovery of sensation may take up to 9 h. 

➧ The lengths of time vary with the agent, the dose, and the volume of LA given. Bupivacaine lasts longer than lidocaine. 

Management: 

a) Precautions: 

1-A test dose of LA is recommended. 

2-The injection of 3 ml of LA containing epinephrine 1:200 000, followed by an adequate pause to assess the effects, has been suggested. 

3-It has been recommended that, if a dural puncture occurs during active labor when a cesarean section is required, then further attempts should not be made. Either a spinal or a general anesthetic should be employed as an alternative. 

b) If Total Spinal a. occurs: 

1-Call for help. 

2-A non-pregnant patient should be turned supine, and the legs elevated to encourage venous return. The pregnant patient should be tilted in the lateral position to prevent aortocaval compression

3-The lungs should be inflated with oxygen

4-A tracheal tube can then be inserted. IPPV may have to be continued for up to 2 h, depending upon the LA and the volume used

5-Intravenous fluids should be infused rapidly

6-A vasopressor agent such as Ephedrine IV in 5–10 mg increments up to 30 mg is recommended. Epinephrine (adrenaline) 0.1–0.5 mg may occasionally be required but should preferably be avoided in patients in labor

7-Atropine for bradycardia, use epinephrine if the patient is unstable

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Viscoelastic Measures of Coagulation

Viscoelastic Measures of Coagulation

Introduction:

➧ Viscoelastic measures of coagulation originated and developed in the 1940s.

➧ TEG was developed and first described by Dr. Hellmut Hartert at the University of Heidelberg (Germany) in 1948. The first reported clinical application of the test occurred during the Vietnam War in an attempt to guide transfusions of blood components in injured soldiers. In the 1980s, TEG was found to be beneficial in liver transplant patients, and in the 1990s, was demonstrated to be useful in cardiac surgery. Since then, TEG has evolved into a more commonly used test as more evidence for its clinical efficacy has been attained.

➧ Current technologies are Thromboelastography (TEG), Rotational Thromboelastometry (ROTEM), and Sonoclot, which allow for real-time in-vitro analysis of the kinetics of clot formation, clot strength, and fibrinolysis on whole blood samples.

A) Thromboelastography (TEG):

➧ TEG is a mechanism for assessing coagulation based on the viscoelastic properties of whole blood.

➧ In contrast to traditional, static measurements of hemostasis (PT, aPTT, INR, fibrinogen level, and fibrin degradation products), TEG allows for an assessment of near real-time, in-vivo clotting capacity, providing the interpreter information regarding the shear elasticity and the dynamics of clot development, strength, stability, and dissolution.

➧ TEG provides information about all components of hemostasis (coagulation, platelet function, fibrinolysis) but offers a particular advantage in diagnosing fibrinolysis.

➧ Graphic interpretation of TEG offers an assessment of coagulopathies (Thrombocytopenia, Factor deficiency, Heparin effect, Hypofibrinogenemia, and Hyperfibrinolysis).

➧ Example: Diagnosis of platelet dysfunction can be inferred by the findings of an abnormal thromboelastogram (in particular, a maximum amplitude < 45 mm) in combination with a normal platelet count and normal tests of coagulation.

Principle: (Figure 1)

Figure 1: Principle

➧ To perform a TEG, a citrated sample of whole blood is placed into a heated sample cup with calcium chloride (to overcome the effects of the citrate), kaolin (a negatively charged molecule known to initiate the intrinsic pathway), and cephalins-phospholipids (required for optimal functioning of the extrinsic pathway).

➧ As the sample cup oscillates in a limited arc, the formation of clot results in the generation of rotational forces on a pin suspended from a torsion wire.

➧ Forces translated to the torsion wire are then transmitted to an electrical transducer and displayed on a computer screen, creating a characteristic waveform with numerical measurements of the kinetics of fibrin formation, fibrinolysis, and the strength of the resulting fibrin clot.

➧ Heparinase cups are commonly paired with plain cups to identify a heparin effect (h-TEG).

Rapid TEG (r-TEG):

➧ Rapid TEG (r-TEG) can be completed within 15 min. as compared to 30-45 min. for a standard TEG.

➧ In contrast to a TEG, whole blood samples for an r-TEG can be performed with citrated or non-citrated samples.

➧ Samples utilized for r-TEG are combined with celite (tissue factor activating the extrinsic pathway), and kaolin (activating the intrinsic pathway) +/- calcium chloride as applicable.

TEG Devices:

1-TEG 5000 (Thromboelastograph Hemostasis Analyzer): (Figure 2)

Figure 2: TEG 5000

2-TEG 6S (Haemonetics): (Figure 3)

Figure 3: TEG 6S

➧ This new device no longer uses the ‘pin-in-cup’ technique, as did TEG 5000.

➧ It uses ‘Resonance’ where blood is exposed to a fixed vibration frequency range and the detector measures the vertical motion of blood meniscus under LED illumination and transforms that movement into tracing of clot dynamics. With pre-prepared cartridges, there is no longer any pipetting required.

B) Rotational thromboelastometry (ROTEM):

➧ Unlike traditional TEG, which utilizes a sample cup rotating in a limited arc, ROTEM employs a static sample cup with an oscillating pin/wire transduction system. (Figure 4)

Figure 4: TEG & ROTEM

➧ ROTEM is a more complex diagnostic test than TEG, as it has four channels with different reagents to detect abnormalities in different components involved in coagulation:

1-INTEM: (Phospholipids) for Intrinsic pathway activation.

2-EXTEM: (Tissue factor for Extrinsic pathway activation.

3-HEPTEM: (Heparinase enz. + Phospholipids) for neutralization of heparin

4-FIBTEM: (Cytochalasin D) to inhibit platelet activity to differentiate between hypofibrinogenemia and platelet deficiency.

5-APTEM: (Aprotinin + Tissue factor) predict the clinical effect of fibrinolysis inhibitors in case of hyperfibrinolysis.

6-NATEM: Native whole blood without reagent

➧ The values of analogous TEG and ROTEM parameters are not interchangeable but provide similar interpretations.

ROTEM Devices:

1-ROTEM Delta (ROTEM Whole Blood Haemostasis Analyser): (Figure 5)

Figure 5: ROTEM Delta

2-ROTEM Sigma: (Figure 6)

Figure 6: ROTEM Sigma

Uses:

➧ Viscoelastic point-of-care coagulation devices have been used in trauma and surgical settings to manage blood component transfusions in bleeding and/or coagulopathic patients.

➧ Rapid real-time bedside test with a simple methodology (point-of-care testing)

➧ Qualitative and quantitative assessment of the whole coagulation profile (Interpreted as normo-, hypo-, or hypercoagulable status)

➧ Global assessment of blood coagulability, including coagulation cascade, platelet function, and fibrinolysis

➧ Predict the clinical efficacy of therapeutic agents affecting blood coagulability

➧ Prediction of need for transfusion (maximum amplitude (MA) is a useful predictor in trauma)

➧ Guidance of blood product therapy, transfusion strategy, and decrease in the use of blood products.

➧ Cost-effectiveness and reduction in blood products in Liver transplantation and Cardiac surgery

➧ It May be useful in:

-Trauma (reduction in blood product use and mortality)

-Obstetrics (may decrease transfusion rates)

-Early detection of dilutional coagulopathy

➧ Difficult to interpret in certain situations:

-Low molecular weight heparin (LMWH)

-Warfarin

-Aspirin

-Post cardiac bypass

-Fibrinolysis

-Hypercoagulability

Graphical Presentation of TEG & ROTEM: (Figure 7)

Figure 7: Graphical Presentation of TEG & ROTEM

Parameters of TEG & ROTEM: (Table 1)

➧ R (Reaction time, min.) or CT (Clotting Time, sec.): Is the time from initiation of the test until clot firmness reaches an amplitude of 2 mm, normal range of 5-7 min.

➧ K (Kinetic time, min.) or CFT (Clot Formation Time, sec.): Is a measure of time from the beginning of clot formation until the amplitude reaches 20 mm, and represents the dynamics of clot formation, normal range 1-3 min.

➧ α-angle (degree): This is an angle between the line in the middle of the TEG tracing and the line tangential to the developing “body” of the TEG tracing. The alpha angle represents the acceleration (kinetics) of fibrin build up and cross-linking, normal range of 53-67 degrees.

➧ MA (Maximum Amplitude, mm) or MCF (Maximum Clot Firmness, mm): reflects the strength of the clot which is dependent on the number and function of platelets and its interaction with fibrin, with a normal range of 59-68 mm.

➧ CL30 or LY30 (%) (A30/MA*100): Clot lysis is measured as the decay in MA over 30 min., normal range of 0-8%.

➧ CL60 or LY60 (%) (A60/MA*100): Clot lysis is measured as the decay in MA over 60 min., normal range < 15%.

Table 1: TEG & ROTEM Parameters

Calculated Parameters:

➧ EPL (Estimated Percent Lysis): EPL at 30 min. calculated continuously commencing 30 sec after determination of maximum amplitude. It is continuously calculated for 30 min at which time EPL becomes Lysis 30 (LY30) as described above.

➧ CI (Coagulation Index): (CI = -0.2454R+ 0.0184K + 0.1655MA - 0.0241a - 5.0220), normal range +/- 3

➧ G (Shear Modulus Strength, dynes/cm²): Measures clot firmness, or strength [G=(5000*MA)/(100−MA)]. G values are higher in clots with more platelet-rich and which are held together by stronger fibrin matrices, normal range of 5.3-12.4 dynes/cm².

➧ E (Elasticity Constant, dynes/cm²): This is the normalized value of G; expressed as [(100*A)/(100−A)]. As a result, a normal maximum amplitude (MA) of 50 mm will yield an E value of 100. This parameter is calculated continuously.

➧ TPI (Thrombodynamic Potential Index): E obtained at maximum amplitude (MA) divided by K or EMX/K.

Examples: (Figure 8) & (Figure 9)

Figure 8: Example 1

Figure 9: Example 2

Case 1: (Figure 10)

Figure 10: Case 1

Interpretation & Diagnosis:

➧ Normal TEG

Case 2: (Figure 11)

Figure 11: Case 2

Interpretation & Diagnosis:

➧ Short R (2 min.) and K (0.5 min.), large alpha angle (78 degrees) and MA (79.5 mm), no fibrinolysis:

-Hypercoagulable state.

Treatment:

➧ Depending on the clinical situation: may be treated with anticoagulant drug therapy.

Case 3: (Figure 12)

Figure 12: Case 3

Interpretation & Diagnosis:

➧ Prolonged R (16.5 min.): Delayed clot formation; suspect:

-Heparin effect

-Factor deficiency

Treatment:

➧ Repeat TEG with Heparinase:

-If normal: administer protamine

-If abnormal: administer FFP

Case 4: (Figure 13)

Figure 13: Case 4

Interpretation & Diagnosis:

➧ Small alpha angle (33 degrees) and MA (39 mm): Weak Clot Formation indicative of:

-Hypofibrinogemia and/or Thrombocytopenia/Poor platelet function.

Treatment:

➧ Requires administration of FFP, cryoprecipitate, and platelets.

➧ Adding ReoPro® (Abciximab) to the TEG sample will eliminate platelet function from the TEG tracing. The MA will become a function of fibrinogen activity.

➧ Low fibrinogen activity can be corrected by the administration of cryoprecipitate or FFP.

Case 5: (Figure 14)

Figure 14: Case 5

Interpretation & Diagnosis:

➧ Short R (3 min.) MA borderline (49 mm), LY30 (11.5%):

➧ Poor platelet function and fibrinolysis

Treatment:

➧ Administer platelets and antifibrinolytics.

➧ The antifibrinolytics can be added to the TEG to pre-evaluate their effectiveness.

➧ Repeat the TEG post-treatment.

Case 6: (Figure 15)

Figure 15: Case 6

Interpretation & Diagnosis:

➧ No clot formation; suspect:

➧ Very low clotting factors level

➧ Heparin effect

Treatment:

➧ Repeat TEG with Heparinase:

➧ If TEG normal: reverse heparin with protamine

➧ If TEG is abnormal: administer FFP

C) Sonoclot:

Principle: (Figure 16)

Figure 16: Sonoclot Principle

➧ The Sonoclot analyzer has a hollow, open-ended disposable plastic probe, mounted on an ultrasonic transducer.

➧ The probe vibrates vertically at a distance of 1 µm at a frequency of 200 Hz and is immersed to a fixed depth in a cuvette containing a 0.4-ml sample of whole blood or plasma.

➧ The viscous drag is mechanically impeding the probe-free vibration.

➧ The drag increases as the sample clots and fibrin strands form on the probe tip, and between the probe and the wall of the cuvette, effectively increasing the mass of the probe.

Figure 17: Clot Signature

➧ The increasing impedance to the vibration of the probe as the sample clots is detected by the electronic circuits driving the probe and converted to an output signal, on a paper chart recorder, which reflects the viscoelastic properties of the developing clot.

➧ The continuous output curve, or “Clot Signature” (Figure 17), describes the whole coagulation process in vitro, from the start of fibrin formation, through polymerization of the fibrin monomer, platelet interaction, and eventually to clot retraction and lysis.

Sonoclot Device: (Figure 18)

Figure 18: Sonoclot Analyser

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