Aneasthesiology

EXAM QUESTIONS IN ANESTHESIOLOGY AND CRITICAL CARE

1. Pain. Definition, stages of pain sensation.

1. Pain. Definition, stages of pain sensation.

  

Pain is a distressing feeling often caused by intense or damaging stimuli, such as stubbing a toe, burning a finger, putting alcohol on a cut, and bumping the “funny bone”

stages:

• Transduction: Conversion of pain stimulation to electrical impulse by nociceptors and transfer of it.
• Transmission: Transfer of electrical impulse via the sensory pathway along Spinothalamic tract e.g. lissauer’s tract.
• Modulation: Change of intensity and details of impulse occurs at reticular area of thalamus, which gives emotional components of pain.
• Perception: This occurs in pre-central gyrus, Which translate and interprets the impulse which have been received.

2. Theories of general anesthesia.

General anesthesia are drugs which produce reversible loss of all sensation and consciousness. it can be inhalators or IV.

Theories of General anesthesia

• Lipid solubility: •Von Bibra and Harless, in 1847, were the first to suggest that general anaesthetics may act by dissolving in the fatty fraction of brain cells.
• Major targets- Ligand gated ion channel
• GABA receptor gated CL- channels: •Barbiturates, anaesthetic steroids, benzodiazepines, propofol , etomidate ,volatile agents modulate GABA A receptor
  •Volatile agents alter /potentiate Ligand binding in GABA A receptor

• Water micro crystals: •MILLER postulated that interaction between water and anaesthetic molecule results in an iceberg which stiffens up membrane  & prevents neuronal transmission
• Membrane theory: •Suggested absorbed anaesthetics decrease cell permeability. Cell was rendered less capable to undergo depolarization  and thus inhibited 
• Protein activity: Detailed analysis of anaesthetic–luciferase interactions led to the suggestion that anaesthetic molecules compete with substrate luciferin molecules for binding to the protein hydrophobic pocket

• Thermodynamic

3. Organization of anesthesiology and resuscitation services. Intensive care department.

An intensive care unit (ICU), also sometimes known as a critical care unit, or an intensive therapy department, is a special ward found inside most hospitals. It provides intensive care – treatment and monitoring – for people who are in a critical or unstable, condition.

Patients in ICUs need constant medical support to keep their body functions going.

They may not be able to breathe on their own, and have multiple organ failure, so medical equipment replaces these functions while they recover.

There are several circumstances in which a person may be admitted to intensive care, for example, following surgery, or after an accident, or severe illness. ICU beds are a very expensive and limited resource because they provide specialized monitoring equipment, a high degree of medical expertise, and constant access to highly trained nurses (usually one nurse per each three beds in Belarus).

Some ICUs are attached to units treating specific conditions, such as heart, kidney, liver, breathing, circulation, or nervous disorders. Others specialize in the care of babies (neonatal), children (pediatrics), or deal with severe injury, or trauma.

4. Indications for admission and transfer of patients to ICU.

Indications for ICU hospitalization:

1. Preoperative treatment in case of severe homeostasis disturbances (e.g. water-electrolyte, protein etc.).

2. After major surgery.

3. Acute circulatory failure including all types of shock.

 

4. Acute respiratory failure.

5. Acute renal failure.

6. Acute hepatic failure.

7. Acute CNS disturbances (severe head or spine trauma, coma, psychosis).

8. Acute metabolic disturbances (e.g. diabetic comas). 

9. Acute coagulation disturbances (DIC-syndrome).

10. Severe infection (sepsis).

11. Polytrauma. 

N.B. ICU beds are expensive and limited, that’s why it is really important to understand that only treatable conditions are supposed to be admitted to an ICU. 

5. Anesthesiology and resuscitation (definitions, goals and objectives).

 6. Classification of modern methods of anesthesia.

7. Methods of objective monitoring of the patients used in anesthesiology and critical care medicine. 

8. Components of general anesthesia.

Components of a general anaesthetic 

   A general anaesthetic always involves an hypnotic agent, usually an analgesic and may also include muscle relaxation. The combination is referred to as the ‘triad of anaesthesia’. 

    The relative importance of each component depends on surgical and patient factors: the intervention planned, site, surgical access requirement and the degree of pain or stimulation anticipated. The technique is tailored to the individual situation

9. Stages of general anesthesia. Classification by Gvedel. 

1 ANALGESIA -Analgesic drugs act in various ways on the peripheral and central nervous systems. They are distinct from anesthetics, which reversibly eliminate sensation.

2 EXCITATION - excitement stage, is the period following loss of consciousness and marked by excited and delirious activity. During this stage, the patient'srespiration and heart rate may become irregular. In addition, there may be uncontrolled movements, vomiting, suspension of breathing, and pupillary dilation.

Because the combination of spastic movements, vomiting, and irregular respiration may compromise the patient's airway, rapidly acting drugs are used to minimize time in this stage and reach Stage 3 as fast as possible.

3 SURGICAL -

 the skeletal muscles relax, vomiting stops, respiratory depression occurs, and eye movements slow and then stop. The patient is unconscious and ready for surgery.it included

  3A “rolling eyes, pupils narrow”

  3B “reflexes lost (respiratory system), pupils partially dilated” – ideal for surgery

  3C “shallow  abdominal respiration, pupils completely dilated” – overdose

4 MEDULLARY DEPRESSION– lethal overdose-

patient has severe brainstemor medullary depression, resulting in a cessation of respiration and potential cardiovascular collapse.

10. Premedication as a component of general anesthesia.

Prior to administration of a general anaesthetic, the anaesthetist may administer one or more drugs that complement or improve the quality or safety of the anaesthetic.

One commonly used premedication is clonidine, an alpha-2 adrenergic agonist.^[4][5] Clonidine premedication reduces the need for anaesthetic induction agents, for volatile agents to maintain general anaesthesia, and for postoperative analgesics.^{[citation needed]} It also reduces postoperative shivering, postoperative nausea and vomiting, and emergencedelirium.^{[citation needed]} In children, clonidine premedication is at least as effective as benzodiazepines and has less serious side effects.^{[citation needed]} However, oral clonidine can take up to 45 minutes to take full effect,^[6] and drawbacks include hypotension and bradycardia.

MAY BEGIN SEVERAL DAYS PRIOR TO SURGERY

PURPOSES

1. SEDATION -is the reduction of irritability or agitation by administration of sedativedrugs, generally to facilitate a medical procedure or diagnostic procedure. Drugs which can be used for sedation include propofol, etomidate, ketamine, fentanyl, and midazolam.

2. PARASYMPATHETIC BLOCK -agent is a substance or activity that reduces the activity of the parasympathetic nervous system.

to prevent from decreasing of heart rate below the lower border. And to reduce the mucous production in the airways.

3. ALLERGY PREVENTION -

4. PAIN MANAGEMENT -loss of pain

5. STOMACK CONTENT ACIDITY MANAGEMENT-

DRUGS

1. BENZODIAZEPINES, CLONIDINE

2. CHOLINOBLOCKERS

3. ANTIHISTAMINES

4. PAINKILLERS

5. H2-BLOCKERS, PROTON PUMP INHIBITORS

11. Inhalatory anesthesia. Definition, volatile anesthetics. 

12. Non-inhalatory methods of general anesthesia. 

13. Multi-component balanced anesthesia.

14. Neuroleptanalgezia. Aspects of the application.

15. Ataralgezia.

16. Total intravenous anesthesia.

17. Conductive anesthesia (definition, classification, indications for use).

18. Indications for the general and local anesthesia.

19. Peculiarities of the preparation of patients for emergency surgery.

20. Preoperative preparation of patients with diabetes.

21. Peculiarities of preoperative preparation of patients with pathology of the cardiovascular system (ischemic heart disease, hypertension, cardiac arrhythmias).

22. Preoperative examination of the patient. The classification of anesthetic risk by AAA.

23. Peculiarities of preoperative preparation of patients with impaired respiratory function.

24. Preoperative preparation of patients with acute blood loss. The choice of method of anesthesia.

25. Anesthesia in ambulatory practice.

26. Pain management of birth labor.

27. Peculiarities of anesthesia for caesarean section.

28. Fentanyl pharmacology.

29. Droperidol pharmacology.

30. Benzodiazepines pharmacology.

31. Muscular relaxants in anesthesiology.

32. Nitrous oxide pharmacology.

33. Volatile anesthetics pharmacology (isoflurane, sevoflurane).

34. Complications during anesthesia.

Important complications of general anaesthesia

• Pain.
• Nausea and vomiting - up to 30% of patients.
• Damage to teeth - 1 in 4,500 cases.
• Sore throat and laryngeal damage.
• Anaphylaxis to anaesthetic agents - figures such as 0.2% have been quoted.
• Cardiovascular collapse.
• Respiratory depression.
• Aspiration pneumonitis - up to 4.5% frequency has been reported; higher in children.
• Hypothermia.
• Hypoxic brain damage.
• Nerve injury - 0.4% in general anaesthesia and 0.1% in regional anaesthesia.
• Awareness during anaesthesia - up to 0.2% of patients; higher in obstetrics and cardiac patients.
• Embolism - air, thrombus, venous or arterial.
• Backache.
• Headache.
• Idiosyncratic reactions related to specific agents - eg, malignant hyperpyrexia with suxamethonium, succinylcholine-related apnoea.
• Iatrogenic - eg, pneumothorax related to central line insertion.
• Death.

Important complications of regional anaesthesia

• Pain - 25% of patients still experience pain despite spinal anaesthesia.
• Post-dural headache from cerebrospinal fluid (CSF) leak.
• Hypotension and bradycardia through blockade of the sympathetic nervous system.
• Limb damage from sensory and motor block.
• Epidural or intrathecal bleed.
• Respiratory failure if block is 'too high'.
• Direct nerve damage.
• Hypothermia.
• Damage to the spinal cord - may be transient or permanent.
• Spinal infection.
• Aseptic meningitis.
• Haematoma of the spinal cord - enhanced by use of LMWH pre-operatively.
• Anaphylaxis.
• Urinary retention.
• Spinal cord infarction.
• Anaesthetic intoxication.
• 
  

35. Early postanesthetic complications.

36. Ketamine pharmacology.

37. Propofol pharmacology.

38. Short-acting barbiturates in anesthesiology.

Mechanism: enhances GABAergic transmission

Uses: Anti convulsive

          Anti anxiety

         Anaethesia

39. Complications of endotracheal anesthesia.

40. Spinal analgesia and anesthesia.

It is the injection of local anaesthetics into the subarachnoid space with a 9mm syringe to bring about aneasthesia or analgsia to the patient from the waist down.

Uses: Surgeries that take place from the hip downwards e.g knee. hip, C.S

contraindication: local infection, anatomical disorder of spine, hypovolemia, bleeding disorders

It is done below L2 vertebra, between L3 and L4 vertebrae.

41. Pain management in the postoperative period.

Non pharmacological:

Explaining to the patient what to expect after surgery

Comfortable bed position

Relaxation therapy

Accupuncture

Transcutaneous electrical nerve stimulation

Pharmacological: 4 class used

Opiods: morphine, fentanyl

adverse effects: ventilation depression, depression of respiratory guard reflex, nausea, vomiting

NSAIDs: Ibuprofen, ketorolac , paracetamol 

Nitric oxide

Local aneasthetics: lidocaine and bupivacaine

42. Epidural anesthesia.

It's the injection of local anaesthetics (more commonly in combination with opoids) into the epidural space to bring about analgesia in small doses and aneasthesia in high doses.

Uses: 

• Vascular surgery - Lower limbs, amputations
• Obstetrics - Cesarean delivery
• Gynecology - Surgeries of female pelvic organs
• Urology - Prostate and bladder surgeries
• General surgery - Lower abdominal surgeries, including appendectomy, bowel surgeries, hernia repair

analgesia 

• Prolonged postoperative analgesia obtained by continuous or patient-controlled infusions of local anesthetics, opioids, adjuvants, or a combination thereof
• Labor epidural analgesia
• Chronic pain management
• 
  

Drugs: Ropivacaine (drug of choice), Bupivacaine (drug of choice for spinal), lisocaine

Opoids: Morphine, fentanyl

43. Acute respiratory failure - definition, classification, etiology.

Definition

Respiratory failure is a syndrome in which the respiratory sys-tem fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination in the normal work of breathing. In prac-tice, respiratory failure is defined as a PaO2 value of less than 60 mm Hg while breathing air or a PaCO2 of more than 50 or less than 30 mm Hg. Furthermore, respiratory failure may be acute or chronic. While acute res-piratory failure is characterized by life-threatening derangements in arterial blood gases and acid-base status, the manifestations of chronic respiratory failure are less dramatic and may not be as readily apparent. Classification of respiratory failure Respiratory failure may be classified as hypoxemic (failure to oxy-genate) or hypercapnic (failure to ventilate) and may be either acute or chronic. Hypoxemic respiratory failure (type I) is characterized by a PaO2 of less than 60 mm Hg with a normal or low (less than 30 mm Hg) PaCO2. This is the most common form of respiratory failure, and it can be asso-ciated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units. Some examples of type I respira-tory failure are cardiogenic or noncardiogenic pulmonary edema, pneumo-nia, and pulmonary hemorrhage. Hypercapnic respiratory failure (type II) is characterized by a PaCO2 of more than 50 mm Hg. Actually the process of CO2 elimination is called ventilation. Hypoxemia is common in patients with hypercapnic respirato-ry failure who are breathing room air. The pH depends on the level of bi-carbonate, which, in turn, is dependent on the duration of hypercapnia. Common etiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (e.g., asthma, chronic ob-structive pulmonary disease [COPD]).

Pathophysiology

Respiratory failure can arise from an abnormality in any of the com-ponents of the respiratory system, including the airways, alveoli, CNS, pe-ripheral nervous system, respiratory muscles, and chest wall. Patients who

have hypoperfusion secondary to cardiogenic, hypovolemic, or septic shock often present with respiratory failure. Hypoxemic respiratory failure: The pathophysiologic mechanisms that account for the hypoxemia observed in a wide variety of diseases are ventilation-perfusion (V/Q) mismatch and shunt. These 2 mechanisms lead to widening of the alveolar-arterial oxygen difference, which normally is less than 15 mm Hg. That means that normally partial pressure of oxygen in alveolar air is pretty close to one in arterial blood. An intrapulmonary or intracardiac shunt causes mixed venous (deoxygenated) blood to bypass ventilated alveoli and results in venous admixture. The distinction between V/Q mismatch and shunt can be made by assessing the response to oxygen supplementation or calculating the shunt fraction following inhalation of 100% oxygen. In most patients with hypoxemic respiratory failure, these 2 mechanisms coexist. Hypercapnic respiratory failure. At a constant rate of carbon dioxide production, PaCO2 is determined by the effectiveness of alveolar ventila-tion (Va). A decrease in alveolar ventilation can result from a reduction in overall (minute) ventilation or an increase in the proportion of dead space ventilation. A reduction in minute ventilation is observed primarily in the setting of neuromuscular disorders and CNS depression. In pure hypercap-nic respiratory failure, the hypoxemia is easily corrected with oxygen ther-apy.

44. Clinical death. Definition, mechanisms of circulatory arrest.

45. Cardiopulmonary resuscitation – stages and steps.

 46. Acute myocardial infarction. Diagnosis and treatment.

47. Unstable angina - diagnosis and intensive therapy.

 48. Ventricular fibrillation. Clinical manifestation, diagnosis and treatment.

49. Brain death. Diagnostics, the value in modern medicine.

50. Decortication.

( social death, awake coma, vegetative condition). Loss of functional activity of the cortex.

51. Postresuscitation desease – clinical manifestations and treatment.

52. Acute pulmonary edema. Clinical manifestations, intensive care.

53. Hypertensive crisis. Methods of intensive care.

54. Stroke (ischemic and hemorrhagic). The differences in the tactics of intensive care.

55. Indications to transfer patients to mechanical ventilation.

56. Blood gases and acid-base balance analysis in intensive care. The value in the diagnosis of respiratory and metabolic disorders.

57. Intensive treatment of acute massive blood loss.

58. Mendelson syndrome prevention.

In 1946 Curtis Lester Mendelson wrote an article entitled "The aspiration of stomach contents into the lungs during obstetric anaesthesia", in the American Journal of Obstetrics and Gynaecology

Prevention

Preventative measures may be applied in labour (particularly in patients at risk of having a caesarean section), before caesarean section and postpartum (for example, with anaesthesia for retained placenta) and include:

• Avoidance of general anaesthesia where possible, particularly for high-risk patients - for example, by use of regional anaesthesia, epidurals, etc.[5] 
• Oral alkalis in labour to reduce pH of stomach contents. Different drugs and preparations have been used alone or in combination, with the aim of raising pH above 2.5 and reducing volume of gastric contents below 25 ml. It is assumed that this will reduce the risk of aspiration. Drugs used include:
  • Magnesium trisilicate: this was used a lot in the past but concerns were expressed about aspiration of particulate antacids and it is used less often.[11] 
  • Sodium citrate: this is used more often in labour and before caesarean section. It is effective at elevating gastric pH but not at reducing gastric volume.[4][11] 
  • H2 inhibitors: a Cochrane review supported the use of H2 inhibitors such as ranitidine or cimetidine and found that they were more effective when combined with antacids.[12] Ranitidine given parenterally has an onset of action of one hour, is as effective as cimetidine given by the same route but lasts longer and causes fewer side-effects.[13] A meta-analysis concluded that H2 inhibitors were more effective in reducing gastric acid volume and gastric pH than proton pump inhibitors.[14] 
  • Metoclopramide: this is traditionally given IV during a caesarian anaesthetic but evidence for its effectiveness in reducing the risk of gastric aspiration is poor.[4] 
• Good anaesthetic technique including:
  • Rapid Sequence Induction (RSI):[4] 
  • The patient should be on a tilting trolley, with suction to hand.
  • Oxygen should be given for three minutes followed by the administration of an induction agent.
  • Cricoid pressure (Sellick's manoeuvre) should be performed. The aim is to compress the oesophagus between the cricoid ring cartilage and the sixth cervical vertebral body thus preventing reflux of gastric contents. The force should be enough to close the oesophagus without distorting the airway.
  • The rapidly acting muscle relaxant, succinylcholine, should be given.
  • Identifying patients likely to be difficult to intubate. Patients can be identified according to certain characteristics - eg, short neck, history of sleep apnoea, previous difficult intubation, etc. A clinical scoring system has been devised.[15] 
  • Compliance with and training in a 'failed intubation procedure'.
  • Identification of patients at risk of aspiration.[16] 

59. Cardiogenic shock. Etiopathogenesis, clinical picture, intensive care.

60. Anafilactic shock.

61. Traumatic shock.

62. Intensive therapy in drowning, strangulation.

63. Sepsis in the intensive care hospitals. Definition, classification.

64. Clinical picture and diagnosis of sepsis.

65. Septic shock.

66. Intensive therapy of sepsis

67. Methods of oxygen therapy.

68. Mechanical lung ventilation: indications, methods

MECHANICAL VENTILATIONINDICATIONS

1.Cardiac arrest/CPR

2.Loss of consciousness (drop below 10 on GCS)

3.Apnea/Bradypnea< 5/min

4.Tachypnea> 30/min with additional respiratory muscles involvement and > 40/min without

5.Cyanosis

6.Tachycardia > 90/min or bradycardia< 45/min associated with hypoxia

7.Hypoxemia: SpO2 < 90% on 150% MV oxygen via mask PaO2 < 55 mmHg on 150% MV oxygen via mask

8.Hyper/Hypocapnia25 > PaCO2 > 60 mmHg

MECHANICAL VENTILATIONMETHODS

1.Mouth-to-mouth

2.Mouth-to-mouth with additional airway (S-curve tube)

3.Facial mask + AMBU bag

4.Facial/nasal mask + Ventilator

5.Endotrachealtube + AMBU bag

6.Endotrachealtube + Ventilator

69. Regimens of mechanical ventilation, methods of respiratory phase shift 


Regimens of mechanical ventilation

1. .—Assist-Control Ventilation Volume Control
2. Assist-Control Ventilation Pressure Control

—A set tidal volume (if set to volume control) or a set pressure and time (if set to pressure control) is delivered at a minimum rate

—Additional ventilator breaths are given if triggered by the patient

3.—Pressure Support Ventilation

—The patient controls the respiratory rate and exerts a major influence on the duration of inspiration, inspiratory flow rate and tidal volume

4. —Synchronized Intermittent Mandatory Ventilation Volume Control

—

5. Synchronized Intermittent Mandatory Ventilation Pressure Control

—Breaths are given are given at a set minimal rate, however if the patient chooses to breath over the set rate no additional support is given

—One advantage of SIMV is that it allows patients to assume a portion of their ventilatory drive

—SIMV is usually associated with greater work of breathing than AC ventilation and therefore is less frequently used as the initial ventilator mode

—Like AC, SIMV can deliver set tidal volumes (volume control) or a set pressure and time (pressure control)

—Negative inspiratory pressure generated by spontaneous breathing leads to increased venous return, which theoretically may help cardiac output and function 

Mechanical Ventilation- Phase Variables

Above is the flow curve generated by the ventilator when delivering a breath in assist control ventilation.

This has a number of phases which can be described, and will help us understand some of the principles of ventilation.

1. Start of inspiration

2. Inspiratory phase

3. End inspiration

4. Expiration

What is it that dictates when the ventilator moves between these phases.

This process will depend upon three different types of phase variables:

Trigger- What is it that causes the start of inspiration?

Limit- limited during inspiration, but does not cycle the breath. So it does not cause the breath to end.

Cycle- what causes the breath to go from end of inspiration to the start of expiration. Or what cycles inspiration? For example is there a certain pressure that needs to be reached or have we set a particular volume that needs to be delivered?

To demonstrate this principle lets talk about the differences between controlled breaths and assisted breaths in volume controlled ventilation.

Controlled breaths

So the trigger variable in controlled breaths, i.e. whats starts inspiration, is time. Every time 6 seconds passes by, if the rate is 10 breaths per minute, another breath is triggered.

The limit variable would be, for example, the flow rate we set. So if we set a flow rate of 60 l/min then this is what will be reached during inspiration and it will go no higher.

What cycles the breath, i.e. what moves us from inspiration to expiration, is volume. When the set volume is reached, for example 500 mls we change to expiration. So the cycle variable is volume.

Assisted breaths

The trigger variable with the assisted breath will not be time but would be initiated by the patient. The ventilator will be set to register if the patient triggers a certain amount of flow e.g. 3 l/min. The ventilator can also be set to detect a certain pressure change generated by the pressure. So the trigger variable with an assisted breath can be either flow or pressure.

The limit variable will still be flow and the cycle variable will still be the volume.

70. Acid-base balance. Principles of correction of metabolic acidosis.

5.6.1 Treatment Principles

The most important approach to managing a metabolic acidosis is to treat the underlying disorder. Then with supportive management, the body will correct the acid-base disorder. Accurate analysis & diagnosis is essential to ensure the correct treatment is used. Fortunately, in most cases this is not particularly difficult in principle. Remember though that a patient with a severe metabolic acidosis may be very seriously ill and even with optimal management the patient may not survive.

The ECLS Approach to Management of Metabolic Acidosis 1. Emergency: Emergency management of immediately life-threatening conditions always has the highest priority. For example, intubation and ventilation for airway or ventilatory control; cardiopulmonary resuscitation; severe hyperkalaemia 2. Cause: Treat the underlying disorder as the primary therapeutic goal. Consequently, accurate diagnosis of the cause of the metabolic acidosis is very important. In some cases (e.g. methanol toxicity) there may be a substantial delay become the diagnosis can be confirmed so management must be based on suggestive evidence otherwise it will be too late. 3. Losses Replace losses (e.g. of fluids and electrolytes) where appropriate. Other supportive care (oxygen administration) is useful. In most cases, IV sodium bicarbonate is NOT necessary, NOT helpful, and may even be harmful so is not generally recommended. 4. Specifics There are often specific problems or complications associated with specific causes or specific cases which require specific management. For example: Ethanol blocking treatment with methanol ingestion; rhabdomyolysis requires management for preventing acute renal failure; haemodialysis can remove some toxins.

Some examples of specific treatments for underlying disorders:

• Fluid, insulin and electrolyte replacement is necessary for diabetic ketoacidosis
• Administration of bicarbonate and/or dialysis may be required for acidosis associated with renal failure
• Restoration of an adequate intravascular volume and peripheral perfusion is necessary in lactic acidosis.

The detailed treatment of the various specific disorders is not considered here, but the important message is that the treatment of each underlying disorder differs so an accurate diagnosis is essential for selection of correct treatment. Treatment of the underlying disorder will result in correction of the metabolic acidosis (ie the bicarbonate level will return to normal).

71. Disseminated intravascular coagulation – etiopathgenesis, stages, diagnosis, treatment.

Etiology

DIC usually results from exposure of tissue factor to blood, initiating the coagulation cascade (see Figure: Fibrinolytic pathway.). DIC occurs most often in the following clinical circumstances:

• Complications of obstetrics (eg, abruptio placentae, saline-induced therapeutic abortion, retained dead fetus or products of conception, amniotic fluid embolism): Placental tissue with tissue factor activity enters or is exposed to the maternal circulation.
• Infection, particularly with gram-negative organisms: Gram-negative endotoxin causes generation or exposure of tissue factor activity in phagocytic, endothelial, and tissue cells.
• Cancer, particularly mucin-secreting adenocarcinomas of the pancreas and prostate and acute promyelocytic leukemia: Tumor cells express or release tissue factor.
• Shock due to any condition that causes ischemic tissue injury and release of tissue factor.

Less common causes of DIC include severe tissue damage due to head trauma, burns, frostbite, or gunshot wounds; complications of prostate surgery that allow prostatic material with tissue factor activity (along with plasminogen activators) to enter the circulation; venomous snake bites in which enzymes enter the circulation, activate one or several coagulation factors, and either generate thrombin or directly convert fibrinogen to fibrin; profound intravascular hemolysis; and aortic aneurysms or cavernous hemangiomas (Kasabach-Merritt syndrome) associated with vessel wall damage and areas of blood stasis.

Slowly-evolving DIC typically results mainly from cancer, aneurysms or cavernous hemangiomas.

Stages of DIC

1. Hypercoagulable stage

2. Consuming hypocoagulable stage

3. Secondary Fibrinolytic stage

Diagnosis

• Platelet count, PT, PTT, plasma fibrinogen, plasma d-dimer

DIC is suspected in patients with unexplained bleeding or venous thromboembolism, especially if a predisposing condition exists. If DIC is suspected, platelet count, PT, PTT, plasma fibrinogen level, and plasma d-dimer level (an indication of in vivo fibrin deposition and degradation) are obtained.

Slowly evolving DIC produces mild thrombocytopenia, a normal to minimally prolonged PT (results are typically reported as INR) and PTT, a normal or moderately reduced fibrinogen level, and an increased plasma d-dimer level. Because various disorders stimulate increased synthesis of fibrinogen as an acute-phase reactant, a declining fibrinogen level on 2 consecutive measurements can help make the diagnosis of DIC. Initial PTT values in slowly evolving DIC may actually be shorter than normal, probably because of the presence of activated coagulation factors in the plasma.

Severe, rapidly evolving DIC results in more severe thrombocytopenia, more prolonged PT and PTT, a rapidly declining plasma fibrinogen level, and a high plasma d-dimer level.

A factor VIII level can sometimes be helpful if severe, acute DIC must be differentiated from massive hepatic necrosis, which can cause similar abnormalities in coagulation studies. The factor VIII level is elevated in hepatic necrosis because factor VIII is made in hepatocytes and released as they are destroyed; factor VIII is reduced in DIC because of the thrombin-induced generation of activated protein C, which proteolyses the activated form of factor VIII.

Treatment

• Treatment of cause
• Possibly replacement therapy (eg, platelets, cryoprecipitate, fresh frozen plasma, natural anticoagulants)
• Sometimes heparin

Immediate correction of the cause is the priority (eg, broad-spectrum antibiotic treatment of suspected gram-negative sepsis, evacuation of the uterus in abruptio placentae). If treatment is effective, DIC should subside quickly. If bleeding is severe, adjunctive replacement therapy is indicated, consisting of platelet concentrates to correct thrombocytopenia; cryoprecipitate to replace fibrinogen and factor VIII; and fresh frozen plasma to increase levels of other clotting factors and natural anticoagulants (antithrombin, proteins C, S, and Z). The effectiveness of infusion of concentrates of antithrombin in severe, rapidly evolving DIC is unresolved.

Heparin is useful in the treatment of slowly evolving DIC with venous thrombosis or pulmonary embolism. Heparin usually is not indicated in rapidly evolving DIC with bleeding or bleeding risk, except in women with a retained dead fetus and evolving DIC with a progressive decrease in platelets, fibrinogen, and coagulation factors. In these patients, heparin is administered for several days to control DIC, increase fibrinogen and platelet levels, and decrease excessive coagulation factor consumption. Heparin is then stopped and the uterus evacuated.

72. Parenteral feeding. Definition, calculation of the energetic value, the method of implementation.

Definition

Parenteral nutrition (PN) is the feeding of a person intravenously, bypassing the usual process of eating and digestion. The person receives nutritional formulae that contain nutrients such as glucose, amino acids, lipids and added vitamins and dietary minerals. It is called total parenteral nutrition (TPN) or total nutrient admixture (TNA) when no significant nutrition is obtained by other routes.

Calculation of Dextrose Content

To determine kcalories supplied from dextrose in the TPN solution, you must first calculate grams of dextrose. Multiply the total volume of dextrose soln (in ml) supplied in a day by the dextrose concentration. This gives you grams of dextrose supplied in a day. Multiply the grams of dextrose by 3.4 (there are 3.4 kcal/g dextrose) to determine kcalories supplied by dextrose in a day.

Note:
If the total dextrose volume is not stated in the prescription, you can calculate it. Just multiply the rate of infusion of dextrose by 24 hr.

*Remember that 1 ml = 1 cc.

Calculation of Protein Content

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To calculate the grams of protein supplied by a TPN solution, multiply the total volume of amino acid solution (in ml*) supplied in a day by the amino acid concentration.Note: If the total volume of AA is not stated in the prescription, you can calculate it. Just multiply the rate of infusion of AA by 24 hr. *Remember that 1 ml = 1 cc

Calculation of Lipid Content

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Since lipid emulsions contain glycerol, the lipid emulsion does not have 9 kcal per gram* as it would if it were pure fat. To determine kcalories supplied by lipid, multiply the volume of 10% lipid (in ml) by 1.1; multiply the volume of 20% lipid (in ml) by 2.0.If lipids are not given daily, divide total kcalories supplied by fat in one week by 7 to get an estimate of the average fat kcalories per day.

Central or Peripheral Veins are used

Hypertonic Solutions

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Peripheral parenteral nutrition feedings usually supplement enteral feedings. Large amounts of nutrients cannot be supplied via a peripheral vein, because these relatively small veins cannot tolerate the rush of fluid into the vein that occurs when a hypertonicsolution is introduced into the circulatory system.

Body fluids have an osmolarity of about 300 mOsm. The introduction of a hypertonic solution into a body compartment will cause an osmotic gradient, resulting in a fluid shift.

73. Drainage of major vessels in intensive care.

74. The principles of poisoning treatment.

Supportive measures should supersede all other considerations in the management of the poisoned patient. The ABC's always come first. Subsequently, the focus may switch to confirmation of a toxic ingestion and specific management issues.

The majority of poisoned patients only require supportive therapy alone in order to recover. Supportive measures alone (Scandinavian method) including mechanical ventilation and circulatory support will permit survival of most patients who are alive upon arrival at the hospital.

In general, the use of antidotes or specific measures should be limited to those patients with clear indications.

Immediately after establishing iv access, a"coma cocktail"of dextrose, thiamine, naloxone and oxygen should be given to all patients with altered mental status. Hypoglycemia must always be a consideration in the unconscious or poisoned patient. Thiamine should be given routinely to all alcoholics or malnourished patients with altered mental status. Naloxone should be considered in all with respiratory depression. Flumazenil rarely, if ever, has to be given emergently, and more careful consideration of its use should be made.

It is important to seek history from sources other than the patient who is often an unreliable historian. These sources include family, friends, the prescribing physician, pharmacists, pre-hospital care personnel, police, and pill bottles or drug paraphernalia at the scene

Attempt to establish the time and size of the ingestion and thus the likelihood that a potentially lethal quantity was ingested. Also try to determine if the patient has vomited spontaneously as this will decrease the need for gastric emptying procedures.

The vital signs are the most important clues to the diagnosis of poisoning and should be measured often and accurately.

The physical exam should focus on identifying a"toxidrome"or toxic syndrome. This is a pattern of signs and symptoms that suggests a specific class of poisoning and allows one to narrow the differential diagnosis. This provides a starting point for management and may suggest the laboratory tests that follow. However, it should be kept in mind that there are many exceptions to the toxidromes and that polydrug ingestions can present with a confusing variety of mixed and overlapping syndromes.

The physical exam should also include evaluation for head trauma, focal neurologic findings, needle track marks, chest auscultation for signs of aspiration or non-cardiogenic pulmonary edema, and unusual odors on the patients breath.

Toxicology screening provides direct evidence of ingestion (although false positives and false negatives do occur), but rarely impacts upon initial management. Initial management should never await results of such analysis.

75. Methods of extracorporeal detoxification.

Check number 90

76. Hemodialysis in the complex treatment of poisoning. The principle of the method, indications and contraindications for use.

Hemodialysis (HD) • Toxins & other substances are cleared from the blood by diffusion across a semi-permeable membrane down a concentration gradient from blood to dialysate • Toxic substance must be water soluble, have low MW, low protein binding, and low volume of distribution • Clearance of the toxin depends on membrane surface area (& type), blood and dialysate flow rated • High-flux membranes can also remove higher MW toxins • Risk for post-HD “rebound” due to redistribution of toxin 

Continuous techniques 

Continuous hemofiltration (CVVH, CVVHD) • Blood passes through large hollow pore fibers, allowing convective removal of molecules up to 40kDa. • Useful in unstable patients • Prolonged duration of therapy, minimizes rebound effects • Disadvantages however include lower clearance vs. HD • CVVH with post-dilution, clearance is equal to UF flow rate (usually not > 4L / hr or 67 ml/min (vs. 500 ml/min in HD)

indications

1. General
   1. Low protein binding
   2. Small volumes of distribution
   3. Water solubility
   4. Low Molecular weight
2. Specific (Mnemonic: I STUMBLED)
   1. Isopropanol
   2. Salicylates
   3. Theophylline, Tenormin (Atenolol)
   4. Uremia
   5. Methanol
   6. Barbiturates (e.g. Phenobarbital)
   7. Lithium
   8. Ethylene Glycol
   9. Depakote (esp. if level >500)

77. Peritoneal dialysis. The principle of the method, indications for use, complications.

The principle of the method

The main principle behind the use of peritoneal dialysis are that toxin within the blood compartment will diffuse freely from the peritoneal micro-circulation through the peritoneum into the dialysis fluid within the peritoneal cavity. After a given period of time ( effluent) is then drained out, to be replaced by fresh diasylate. By varying the concentration of diasylate, different volumes of water can be removed (ultrafiltration) with each dialysis exchange, as a result of osmosis.

indications for use

mainly used in renal failure

Strong indications for peritoneal dialysis include the following:^[4]

• Vascular access failure
• Intolerance to hemodialysis
• Congestive heart failure
• Prosthetic valvular disease
• Children aged 0-5 years
• Patient preference
• Distance from a hemodialysis center
• Poor cardiac function
• Peripheral vascular disease

Peritoneal dialysis is preferred in patients with the following conditions:^[4]

• Bleeding diathesis
• Multiple myeloma
• Labile diabetes mellitus
• Chronic infections
• Possibility of renal transplantation in the near future
• Age between 6 and 16 years
• Needle anxiety
• Active lifestyle

Peritoneal dialysis has been utilized infrequently for nonrenal indications with variable benefit in other conditions as follows:^{[5, 6, 7, 8, 9, 10]}

• Refractory congestive heart failure
• Hepatic failure
• Hypothermia
• Hyperthermia
• Hyponatremia
• Dialysis-associated ascites
• Drug poisonings
• Pancreatitis
• Inherited enzyme deficiencies

complications

Bowel perforation

The risk of bowel perforation is less than 1%, and it usually occurs during entry into the abdominal cavity or when the catheter and stylet are advanced into the abdomen. Surgical exploration is necessary with repair of the perforation and removal of the catheter.^[11]

Bleeding

Bleeding is rarely a significant problem after peritoneal dialysis catheter placement. When bleeding occurs, it is usually at the exit site.

Wound infection

Wound infection is uncommon and often can be treated with antibiotics when it is superficial. If the wound is deeper, then it may need to be drained.

Peritonitis

Peritonitis is often the result of contamination with skin bacteria

Encapsulating peritoneal sclerosis

Peritoneal failure

78. Hemosorbtion. Opportunities in the treatment of exo- and endotoxicosis.

Definition:

Hemosorption (. From the Greek haema blood + Latin sorbere absorb.) - A method of treatment aimed at removing from the blood of a variety of toxic products and the regulation of hemostasis by contact with the blood outside the body of the sorbent. Hemosorption - method of extrarenal blood purification from toxic substances by adsorption of poison on the sorbent surface.

Indications for hemosorption:

• withdrawal symptoms when drug addiction, substance abuse, alcoholism;
• manic and depressive states at mental diseases and conditions;
• acute poisoning hypnotic drugs, chlorine and organophosphorus compounds, alkaloids, salicylates, heavy metals.

Contraindications for hemosorption:

• all kinds of bleeding;
• violation of blood coagulation;
• shortage of blood volume;
• persistent hypotension;
• electrolyte disorders;
• hemodynamic instability;
• cardio-pulmonary insufficiency;
• severe liver and kidney function.

Clinical effects:

Efficacy hemosorption system due to rapid detoxification by binding a large number of sorbent dissolved in the blood, the compounds and metabolites. Especially clearly manifested in effect hemosorption alcohol poisoning or its products of metabolism, which is manifested in the elimination of the main ultra-poisoning symptoms - general discomfort, headache, autonomic disorders.

After the first procedure is a significant reduction of pathological concentrations of products, but after several hours the concentration increases and approaches the source of blood. This is explained by the fact that in the bloodstream actively enter the substances dissolved in the tissue and cellular fluids. Subsequent efferent hemosorption procedure ultimately removed pathogens in the body.Causing long-term remission (no symptoms of the disease). Therefore, to achieve a stable positive effect of holding several procedures recommended.

Among the various methods of extracorporeal blood correction hemosorption different technical ease of implementation, compatibility with medical equipment for plasmapheresis. Gemosrbtsiyu distinguishes the circuit simplicity. Use standard equipment for plasmapheresis (devices "Gemos", "Hemofenix", hand pump, etc..), Mass-exchange device (sorbent) and a system of highways.Driving device hemosorption circuit device as an example "Gemos" is shown in Figures 1 and 2.

Fig. 1. Hemosorption	Fig. 2. Driving circuit

The main active component of the circuit is hemosorbent. This granular carbon material subjected to activation demineralization depyrogenation, hydro processing, balancing ion and sterilizing. Hemosorbent used to remove a wide range of low and medium molecular weight, the gram-negative bacterial flora and its endotoxin from the blood of patients.

79. Enterosorbtion. Aspects of the application.

Adsorption of substances from the gastrointestinal tract onto an orally administered sorbent medium like activated charcoal. This technique is used to eliminate toxic and some biologically active substances and serves to modify thelipid and amino acid spectrum of the intestinal contents

80. Forced osmotic diuresis. Indications for use.

Mannitol is used alone or with other diuretics (e.g., furosemide, ethacrynic acid) to promote the urinary excretion of toxins (e.g., aspirin or other salicylates, some barbiturates, bromides, imipramine) as an adjunct to usual treatment regimens in patients with severe intoxications

81. Acute poisonings with mushrooms.

The main causes of mushroom toxicity are as follows:

• Incorrect identification of a mushroom (eg, by a novice mushroom harvester or by someone who mistakes a poisonous local variety for an edible variety that is native to where they learned to pick mushrooms); many species are similar enough in appearance to confuse an inexperienced or insufficiently informed mushroom hunter
• Unintentional ingestion by a child who found mushrooms growing in yards or outdoor play areas
• Intentional ingestion by a person with euphoric intent (substance abuse)

Rare causes are as follows:

• Intentional ingestion by a suicidal person
• Foul play in which an individual is poisoned by someone else
• Inadvertent poisoning from dried mushrooms purchased on the Internet or from other sources for which the composition of the mushroom is unreliable or the mushroom might be contaminated with unknown toxic compounds

Accidental poisoning accounts for more than 95% of the cases of mushroom intoxications; most of the remaining cases are due to intentional ingestion of the mushrooms for their mind-altering properties.

Cyclopeptide (amatoxin) poisoning most commonly is due to the following:

• Amanita species (ie, bisporigera, ocreata, phalloides, tenuifolia, virosa, verna)
• Galerina species (ie, autumnalis, sulcipes, marginata)
• Lepiota species ( brunneoincartata, helveola, josserandii, subincarnata)

TREATMENT

• Pre-hospital: make every attempt to identify the ingested mushroom. In the UK, Toxbase® has descriptions and photographs to help with identification.[1] Care is otherwise supportive.
• Early onset of gastrointestinal symptoms predicts a benign course so nothing more than symptom control may be warranted.
• Consider activated charcoal in those presenting with gastrointestinal symptoms six hours after ingestion or if a patient presents before symptom development following known ingestion of hepatotoxic or nephrotoxic species.
• There is evidence to suggest that multi-dose activated charcoal may be more beneficial in amanita poisonings, as some of the toxins undergo enterohepatic circulation.[4]
• In the UK, contact the National Poisons Information Centre.[5] .
• Observe for six hours to exclude central nervous system (CNS) and gastrointestinal toxicity. Treat symptomatically.
• Atropine for cholinergic symptoms (eg, as with inocybe mushroom toxicity) and pyridoxine for gyromitra.
• The very rare hepatotoxic mushrooms can cause gastrointestinal symptoms from six hours onwards.
• N-acetylcysteine is sometimes used as an antidote for hepatotoxicity associated with mushroom poisoning but the evidence for its effectiveness is limited.

Specific mushroom toxicities

Amanita phalloides

• The most poisonous mushroom toxins are produced byA. phalloides.
• Supportive care, including correction of hypoglycaemia and electrolyte imbalance.
• Gastric lavage and activated charcoal.
• Anecdotal and animal studies suggest a potential benefit of high-dose penicillin, silibinin (a constituent of the extract silymarin derived from the milk thistle, Silybum marianum), cimetidine, aucubin (an iridoid glycoside of Aucuba japonica) and kutkin.
• Fulminant hepatic failure may require a liver transplant

Treatment of muscarine poisoning

The treatment for this symptom complex is atropine titrated to reduce symptoms, induce slight dryness of mouth and restore normal or nearly normal pupil size. The initial adult dose of atropine is 0.5 to 1.0 mg given very slowly intravenously. Repeat doses of 0.5-1.0 mg can be given at 10-20 minute intervals to either of two endpoints: A. 1 mg doses until bronchial hypersecretion, pulmonary edema and significant cardiac arrhythmias have cleared or B. 0.5 mg of atropine until the pupils are normal or nearly so. The second end-point may take longer to achieve; its use requires increased diligence and slower administration of atropine to avoid overdosage. Usually no more than 2.5 mg of atropine is required.

82. Carbon monoxide poisonings.

Sources of carbon monoxide:

• Gas water heaters
• Kerosene space heaters
• Charcoal grills
• Propane heaters and stoves
• Gasoline and diesel powered generators
• Cigarette smoke
• Propane-fueled forklifts
• Gasoline powered concrete saws
• Indoor tractor pulls
• Boats engines
• Spray paint, solvents, degreasers, and paint removers

Treatment

83. Acids and alkalis poisonings.

Caustics (strong acids and alkalis), when ingested, burn upper GI tract tissues, sometimes resulting in esophageal or gastric perforation. Symptoms may include drooling, dysphagia, and pain in the mouth, chest, or stomach; strictures may develop later. Diagnostic endoscopy may be required. Treatment is supportive. Gastric emptying and activated charcoal are contraindicated. Perforation is treated surgically.

Symptoms and Signs

Initial symptoms of caustic ingestion include drooling and dysphagia. In severe cases, pain, vomiting, and sometimes bleeding develop immediately in the mouth, throat, chest, or abdomen. Airway burns may cause coughing, tachypnea, or stridor.

Swollen, erythematous tissue may be visible intraorally; however, caustic liquids may cause no intraoral burns despite serious injury farther down the GI tract.

Esophageal perforation may result in mediastinitis, with severe chest pain, tachycardia, fever, tachypnea, and shock. Gastric perforation may result in peritonitis. Esophageal or gastric perforation may occur within hours, after weeks, or any time in between.

Esophageal strictures can develop over weeks, even if initial symptoms had been mild and treatment had been adequate.

Diagnosis

• Endoscopy

Because the presence or absence of intraoral burns does not reliably indicate whether the esophagus and stomach are burned, meticulous endoscopy is indicated to check for the presence and severity of esophageal and gastric burns when symptoms or history suggests more than trivial ingestion.

Treatment

• Avoidance of gastric emptying
• Sometimes dilution with oral fluids

Treatment of caustic ingestion is supportive. (Caution: Gastric emptying by emesis or lavage is contraindicated because it can reexpose the upper GI tract to the caustic. Attempts to neutralize a caustic acid by correcting pH with an alkaline substance [and vice versa] are contraindicated because severe exothermic reactions may result. Activated charcoal is contraindicated because it may infiltrate burned tissue and interfere with endoscopic evaluation and insertion of an NGT is contraindicated because it can damage already compromised mucosal surfaces .)

Dilution with milk or water is only useful in the first few minutes after ingesting a liquid caustic, but delayed dilution may be useful after ingesting a solid caustic. Dilution should be avoided if patients have nausea, drooling, stridor, or abdominal distention.

Esophageal or gastric perforation is treated with antibiotics and surgery (see Acute Perforation). IV corticosteroids and prophylactic antibiotics are not recommended. Strictures are treated with bougienage or, if they are severe or unresponsive, with esophageal bypass by colonic interposition.

84. Barbiturate poisoning.

Flumazenil competitively and reversibly binds benzodiazepine receptors (ie, GABA).

85. Poisoning with hypnotics.

 Sedative-hypnotics are a group of drugs that cause central nervous system (CNS) depression. Benzodiazepines and barbiturates are the most commonly used agents in this class. Other agents include the nonbarbiturate nonbenzodiazepine sedative-hypnotics.

Most cases of severe sedative-hypnotic poisoning are deliberate (suicidal). These agents are also commonly abused as recreational drugs.

Barbiturates

Ultrashort acting - Methohexital (Brevital) and thiopental (Pentothal)

Short and intermediate acting - Amobarbital (Amytal), pentobarbital (Nembutal), secobarbital (Seconal), butalbital (Fioricet, Fiorinal)

Long acting - Phenobarbital (Luminal)

Nonbarbiturates

Benzodiazepines

Carbamates - Meprobamate (Equanil, Miltown)

Chloral derivatives - Chloral hydrate (Noctec)

Ethchlorvynol (Placidyl)

Piperidines - Glutethimide (Doriden), methyprylon (Noludar)

Quinazolinone - Methaqualone (Quaalude)

Imidazopyridine - Zolpidem (Ambien), zaleplon (Sonata), eszopiclone (Lunesta)

Antihistamines (over-the-counter sleep aids) - Diphenhydramine,d doxylamine

Gamma-hydroxybutyrate (GHB) and its analog gamma-butyrolactone (GBL)

Treatment same as in number 85

86. Acute poisoning with methanol.

87. Bites of snakes and insects – toxicological aspects.

88. Methods of gastric lavage in acute poisoning.

I. Precautions

A.    Gastric Lavage should not be used routinely (if at all) in Poisonings

B.    In rare cases, when indicated, it should only be used by those trained in proper technique

II. Indications

A.    Rarely indicated in 2012

1.      Poor efficacy

2.      Significant nasal Trauma from large bore tubes

B.    Historically used in severe ingestion cases

1.      Overdose or Ingestion within 1 hour

2.      Extraordinary Overdose with a potentially toxic amount of medication

3.      Specific Overdose after 1 hour

a.      Ingested drug slows peristalsis

                                                                         i.            Anticholinergics

                                                                       ii.            Opioids (Narcotics)

b.     Ingested drug forms Bezoar

                                                                         i.            Salicylates

                                                                       ii.            Iron

III. Contraindications

A.    Insignificant Overdose

B.    Corrosive Ingestion (strong acid or alkali)

C.    Hydrocarbon Ingestion (high aspiration risk)

D.   Minimally effective if given >1 hour post-ingestion

E.    Increased risk of Gastrointestinal Bleeding or perforation

F.     Unprotected airway (e.g. Altered Level of Consciousness)

IV. Complications

A.    Aspiration Pneumonia

B.    Laryngeal Trauma

C.    Esophageal Perforation

D.   Epistaxis

E.    Electrolyte imbalance

F.     Hypothermia

V. Preparations

A.    Activated Charcoal in aqueous solution (preferred due to lower Emesis, aspiration risk)

B.    Activated Charcoal in Sorbitol

VI. Technique

A.    Consider Endotracheal Intubation in advance

1.      Indicated for neurologic Impairment

B.    Use a large bore tube (28 French Ewald tube)

1.      Larger tubes however cause considerable nasal Trauma

C.    Position patient

1.      Head down

2.      Left lateral decubitus

D.   Technique

1.      Aspirate first prior to fluid lavage

2.      Instill lavage fluid into Stomach

a.      Adult 100-300 cc warm water or Normal Saline per wash

b.     Child 10-15 cc/kg warm Normal Saline per wash

3.      Aspirate fluid back and dispose of fluid

E.    Repeat lavage

1.      Repeat until aspirate clears of pill fragments and similar debris of concern

2.      Single dose is sufficient in many cases

3.      If repeated, alternate aqueous and Sorbitol charcoal preparations every 2 hours

89. Possibilities of antidote therapy in complex treatment of acute poisoning.

Antidotes may play an important role in the treatment of poisoning. While good supportive care and elimination techniques may, in many cases, restore a poisoned patient to good health and stabilize his or her body functions, the appropriate use of antidotes and other agents may greatly enhance elimination and counteract the toxic actions of the poison. In certain circumstances they may significantly reduce the medical resources otherwise needed to treat a patient, shorten the period of therapy, and, in some cases, save a patient from death. Thus, antidotes may sometimes reduce the overall burden on the health service of managing cases of poisoning. In areas remote from good hospital services, and particularly in developing countries that lack adequate facilities for supportive care, antidotes may be even more essential in the treatment of poisoning.

Physicians frequently express concern about the difficulty of obtaining certain antidotes in an emergency. The IPCS and the EC, in consultation with the World Federation, are undertaking a project designed to evaluate the efficacy of antidotes and to encourage their availability. In a preparatory phase of this project an antidote was defined as a therapeutic substance used to counteract the toxic action(s) of a specified xenobiotic. A preliminary list of antidotes, and of other agents used to prevent the absorption of poisons, to enhance their elimination, and to counteract their effects on body functions, was established; preliminary classification of these agents was based on urgency of treatment and efficacy in practice. Agents that correspond to the WHO concept of an essential drug were designated as such, and some have already been incorporated into the WHO List of Essential Drugs1. Antidotes and substances for veterinary use were also listed. Methods and principles for the evaluation of antidotes and other agents used in the treatment of poisoning were drafted and are being used as a framework for preparing monographs on specific antidotes, which are being published in a special series.2

90. Extracorporeal detoxification methods in the complex of measures of intensive care of acute poisoning.

DEFINITION Group of methods of treatment based on extracorporeal perfusion of patient’s blood through the circuit including detoxifying device (hemofilter, plasmafilter, sorbent etc.)

IDEA OF THE METHOD The method is based on the perfusion of blood through the circuit by roller pump

WHERE TO TAKE BLOOD AND WHERE TO RETURN?

1. Artery → Vein. Not used already. Good perfusion

pressure, but difficult to access and many

complications

2. Peripheral Vein → Peripheral Vein. Easy to access but

low perfusion pressure. Good for slow perfusion

techniques

3. A/V fistula → Peripheral Vein. Good perfusion pressure

and easy to access but necessary to make surgery prior

to use. Good for chronic dialysis

4. Central Vein → Peripheral Vein. Good Perfusion

pressure but necessary to use 2 lines

5. Central Vein → Central Vein (dual lumen catheter).

Method of choice for emergency application

CLASSIFICATION

1. Dialyzing methods

- Hemodialyzis

- Peritoneal dialyzis

- Hemofiltration

- Hemodiafiltration

- Isolated ultrafiltration

2. Plasma exchange

- Gravitational plasmapheresis

- Plasmafiltration

3. Hemosorbtion

- Selective (biospecific, lipid-specific)

- Non-selective (charcoal perfusion)

4. Combined methods

FIELDS OF APPLICATION

1. Chronic renal failure. Dialyzing methods

2. Acute renal failure. Dialyzing methods

3. Acute hepatic failure. Plasma exchange, albumin purification methods, dialyzing methods

4. Acute cardiac failure. Isolated ultrafiltration

5. Severe poisonings. Hemosorbtion, dialyzing methods, plasma exchange

6. Severe endogenic intoxications. Dialyzing methods, hemosorbtion, plasma exchange

7. Severe autoimmune disorders. Plasma exchange

8. Malignant hypertriglyceridemia. Lipid sorbtion

DIALYZING METHODS

Based on the phenomenon of direct osmosis – the movement of substances through the semipermeable membrane via the gradient of concentration from high to low ‘til equalization

DIALYZING METHODS

1. Hemodialyzis – perfusion of blood through capillary dializer washed with dialyzing solution (acute and chronic renal failure)

2. Peritoneal dialyzis – perfusion of dialyzing solution through the patient’s abdomen (peritoneum is a membrane) (outpatient treatment for chronic renal failure)

3. Hemofiltration – perfusion of prediluted blood through capillary dialyzer (severe toxicosis)

4. Hemodiafiltration – perfusion of prediluted blood through capillary dialyzer washed with dialyzing solution (severe toxicosis ± acute renal failure)

5. Isolated ultrafiltration – perfusion of blood through capillary dialyzer (acute fluid overload)

PLASMA EXCHANGE

Based on separation of patient’s plasma, wasting it and substitution with infusion and transfusion medium

- Gravitational plasmapheresis. The blood is separated by the centrifuge, plasma wasted, hemacyte is returned back to patient along with substitutive solutions.

Advantage – speed up to 2000 ml/hr of plasmexfusion

Disadvantages – relatively expensive (≈ 150 eur/set) and technically complicated

- Plasmafiltration. The blood is separated by special plasmafilter, plasma wasted, hemacyte is returned back to patient along with substitutive solutions.

Advantages – technical simplicity, low cost

Disadvatage – slower than gravitational

HEMOSORBTION

Based on the perfusion of patients blood through the sorbent binding toxic

substances and return back to the patient

- Selective (biospecific, lipid-specific)

The sorbent is selectively binding specific group of substances

E.g. - proteinases (“Ovosorb”)

- microbic endotoxin (“Toraymyxin”)

- lipids (“Dali-Art”)

- Non-selective (charcoal perfusion)

COMBINED METHODS

Combine different techniques in one circuit. Used in complicated cases e.g. renal-hepatic failure

Good example: Prometheus by Fresenius Albumin sorbtion + Dialyzis

1. Albumin is separated by albu-filter, than it is liberated from bilirubin and returned back to blood

2. Blood is dialyzed from ammonium

CHOOSING THE METHOD IN ACUTE POISONING

1. Acute toxicogenic stage (non-specific clinical presentation, short time passed after intake)

Charcoal perfusion, hemofiltration, hemodiafiltration – any unknown poison

Dialyzis – water-soluble low molecular weight nonorganic compounds

Plasma exchange – liposoluble high molecular weight organic compounds

2. Somatogenic stage (delayed time after intake, target specific organ failure)

The method is chosen according to the prevailing organ failure (renal or hepatic )