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
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.
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 |
*Remember that 1 ml = 1 cc |
Calculation of Lipid Content |
Central or Peripheral Veins are used
Hypertonic Solutions |
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
- General
- Low protein binding
- Small volumes of distribution
- Water solubility
- Low Molecular weight
- Specific (Mnemonic: I STUMBLED)
- Isopropanol
- Salicylates
- Theophylline, Tenormin (Atenolol)
- Uremia
- Methanol
- Barbiturates (e.g. Phenobarbital)
- Lithium
- Ethylene Glycol
- 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 )
Thanks a lot this is really helpful
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