Comatous states

 

Comatous states

1 Anatomy and physiology of central nervous system.

Nervous system consists of two parts: central nervous system and peripheral nervous system.

The brain (central nervous system, higher vegetative centres and endocrine regulation centres ) is located in the skull – reliable bony container, which protects it from the most dangerous environment factors.

As a central regulator of all body functions brain requires a very high level of metabolic processes. Its weight is just 2 % of the body weight (nearly 1500 grams), however it takes nearly 14-15% of circulating blood volume (700-800 ml) every minute. Brain consumes 20% of total oxygen, which gets to the organism every minute. However its main limitation factor is glucose, because it is the only source of energy for the brain (75 milligrams per minute or 100 grams per day).

Thus, physiologically functions of the central nervous system depend on an adequate perfusion (oxygen and glucose supply) and adequate blood outflow (wastes transportation) from the cranial cavity.

Serious self-regulation system provides uninterrupted brain functioning and even during massive blood loss brain gets its amount of oxygen through the mechanism of blood flow centralization (of course this causes ischemic injury of visceral organs, but their affection evolution quite reasonably considered less harmful). There is also a mechanism which protects brain in case of hypoglycaemia: blood flow increases and thus increases amount of glucose getting to the nervous cells. On the other hand hyperventilation (hypocapnia) decreases blood flow and hypoventilation (hypercapnia) increases it to eliminate acid metabolites.

When brain tissue is much damaged and regulation fails, brain is not able to change its volume according to the needs. So when blood flow and outflow get into the imbalance the protective cranial “bone box” (the skull) actually becomes brain’s main enemy, because it can’t be extended. For example 5% increasing of blood volume (haematoma, tumour, overhydration, liquor hypertension, etc.) causes unconsciousness. Excessive blood flow brings liquor hyperproduction and this causes brain compression and results in brain tissue edema and functional disorders.

Brain injuries, vascular disorders, cerebral oedema, increase of intracranial pressure, liquor circulation violations result in cellular hypoxia of central nervous system. Alerted level of consciousness is the first sign of cerebral hypoxia.

 

5.2 Classification, clinic and diagnostics of coma.

Coma is a complete depression of consciousness with lack of pain sensitivity and reflexes, general muscular relaxation and violated vital functions.

 

Classification of consciousness levels according to Bogolepow, 1982.

Conscious (normal)

Confused

Stuporous

Soporous

Comatose: moderate

                  deep

                  terminal

Each level has its own diagnostic criteria; you can find them in the table below.

 

Levels of consciousness	Main symptoms	General symptoms
Conscious	Alert, absolutely oriented to self, place and time patients.	Attention is active, speech is fluent, answers are correct and full, commands are obeyed, eyes are opened spontaneously.
Confused	Moderate somnolence or euphoria, partial disorientation with the place and time, but complete self orientation.	Thinking and attention are impaired. Verbal contact is slowed; questions should be repeated to receive answers. Commands are obeyed, however slowly, especially complex commands.
Stuporous	Deep somnolence, time and place disorientation, only simple commands are obeyed after awakening.	Most of the time patient sleeps, sometimes however there are periods of restlessness and agitation. Answers are curt. Defensive reaction to pain stimuli is maintained. Pelvic organs control is deficient.
Soporous	Pathologic somnolence; time, space and self disorientation.	Opens eyes in response to painful stimuli, localizes painful stimuli; reflexes of cerebral nerves and vital functions are preserved.
Moderate comatose	Unconscious	No reaction to external stimuli. To painful stimuli answers with withdrawal. Corneal and pupillar reflexes are overactive, abdominal reflexes are reduced. There are pathologic plantar reflexes. Pelvic organs control is violated. Vital functions are preserved.
Deep comatose	Unconscious	Extension to painful stimuli. Skin, tendon, corneal and pupillar reflexes are reduced or absent. Skeletal muscles are rigid or hypotonic. There are respiratory and cardiac disorders.
Deepest comatose	Unconscious	Areflexia, bilateral fixed midriasis, muscle atony; great violations of vital functions. Blood pressure less than 60 mmHg.

 

Classification of coma according to etiology and pathogenesis.

1.         Coma of central genesis (epileptic, traumatic, apoplectic).

2.         Coma caused by visceral organs dysfunctions and endocrine glands disorders (diabetic, hypoglycaemic, thyrotoxic, myxedemic, hypopituitary, hypocorticoid, hepatic, uremic, hypochloremic, anaemic, alimentary-distrophic ).

3.         Infectious coma (in case of pneumonia, malaria, neuronal infections, etc.).

4.         Acute toxic coma (poisonings with alcohol and its surrogates, medicinal poisonings, carbon monoxide poisonings).

5.          Coma caused by physical factors ( caused by electric injury, hypothermic and hyperthermia coma, radiation coma, etc.).

Sometimes it is very hard to find the reason of the coma, so detailed anamnesis (interview relatives and witnesses) and clinical observations are very important.

First of all ask about the duration of unconsciousness and was it lost suddenly or there were other levels of altered consciousness. Ask about the events prior to incident: did the patient fell and was there a chance of head injury? Did he have fever, flu or jaundice? Are there any sings of chronic diseases like diabetes, epilepsy, hypertonic disease? Have the patient ever suffered from similar unconsciousness episodes? Were there any suicide attempts? If the comatose condition was not sudden, have the patient complained of vomiting, convulsions? Pay attention to the personal things of the patient: you can find medical documents, medicine packages, diabetic bracelets or necklaces, etc.

If the anamnesis failed to reveal the coma etiology, concentrate on objective symptoms.

Skin colour: extreme paleness can be a sign of great blood loss, circulatory collapse, blood diseases. Cyanosis is a symptom of hypercapnic coma caused by respiratory failure or asphyxia (hanging, drowning, convulsions). Hyperaemic face allows you to think about atropine and carbon monoxide poisonings, hyperglycaemic coma or infectious disease.

Head position: tilted back head is a sign of meningitis, tetanus, hysteria; head turned aside can be the symptom of stroke.

Pathological types of breathing are also helpful in coma diagnostics: Cheyne-Stokes breathing (periods of apnoea, which are followed with chaotic frequent breathing) and Biot’s breathing (periods of apnoea which are followed with breathing of equal amplitude) show deep affection of central nervous system. Kussmaul breathing (deep and laboured) proves accumulation of acid metabolites (metabolic acidosis) of exogenous (in case of poisonings) or endogenous (diabetic ketoacidosis) nature. Fever and rapid deep breathing are probable signs of infectious coma. Remember that per each excess body temperature degree there are 5-7 excess breathes and 10 excess heart beats.

Generally when you are coming to the patient with consciousness disorders try to do this from the side of patient’s head (nape): this way you can easily improve airways patency if necessary (thrust the jaw forward for example) and avoid accidental injuries from the patient if his moves are uncontrolled.

You can always identify simulation or hysteric coma by opening the eyes of the patient: in case of simulating conscious patients or hysteric patients you will feel the resistance of the eyelids. Unconscious patients never resist when you try to open their eyes.

Pressing the eyeballs toy can evaluate their tone: “soft” eyeballs with decreased tone are the symptom of hypovolemia (bleeding, dehydration) or shock condition. However they can also be part of hyperglycaemic coma clinic.

The depth of coma is assessed with the reflexes reduction. If patient reacts to the external stimuli – it’s a moderate coma. If corneal reflexes are preserved with depressed other reflexes – it’s a deep coma. Lack of photoreaction is a symptom of terminal coma.

Pupil’s diameter varies: pupils are narrowed in case of sleeping pills overdose or organophosphate poisonings; terminally narrow pupils you can see in patients after drugs admission; pupils are dilated in case of hypoxia, neuroleptic poisonings, antihistamine medicines intoxications; the widest pupils you can observe in atropine poisoning.

Anisocoria (pupils of different size) is a symptom of local CNS injuries. In most cases you notice this sign when a trauma causes intracranial haematoma. Examine those patients carefully: look for bruises and scratches on the head (including parts covered with hear). Sometimes you can eveotice eyeballs deviation to the side of injury. Lack of patellar and heelstring reflexes proves deep CNS affection. Pathological Babinski’s reflex shows organic CNS injury. Muscular tone asymmetry is a sign of stroke, tumour, haematoma, etc.

Don’t forget to assess other systems and organs, because brain reaction can be only the response to a serious visceral pathology. For example unconsciousness can be a consequence of cardiac arrhythmia (Morgagni-Adams-Stokes syndrome). And on the contrary: CNS violations can cause rhythm disorders.

 

Localization of the brain pathology	Cardiac symptoms
Damage of frontal lobes and orbital zones	Bradycardia, complete AV block, auricular extrasystole
Damage of midbrain	Extrasystole, atrioventricular block, VF
Medulla oblongata pathology	Node and ventricular extrasystole, fluttering arrhythmia
Hypothalamic zone damage	Extrasystole, paroxysmal tachycardia
Affection of vascular center	Severe vascular tone decrease, hypotension, bradycardia, cardiac arrest.

 

Pericardial murmur and pleural rub can indicate uraemic coma. Changes of liver size are features of hepatic coma. Enlarged spleen is a symptom of bone marrow or liver diseases.

In case of comatose patients use all your laboratory and instrumental possibilities: perform head X-ray, CT, liquor tests, encephalography, angiography, usual blood tests, etc.

 

Pic. 5.1 Lumbar puncture.

 

For assessment of central nervous system condition Glasgow Coma Scale was proposed in 1974.

 

Clinical signs	Points
Eyes opening
Spontaneous	4
In response to voice	3
In response to pain	2
Does not open the eyes	1
Verbal response
Converses normally	5
Confused, disoriented answers	4
Inappropriate words	3
Incomprehensible sounds	2
No sounds	1
Motor response
Obeys commands	6
Localizes painful stimuli	5
Withdrawal to painful stimuli	4
Abnormal flexion to painful stimuli	3
Extension to painful stimuli	2
No movements	1

 

Count the points and assess the result according to this:

13-14 points – moderate confusion

11-12 points – deep confusion

8-10 points – sopor

6-7 points – moderate coma

4-5 points – deep coma

3 points – deepest coma

 

Immediate aid for comatose patients:

–         turn the patient aside

–         thrust the jaw forward

–         assess respiration (skin and mucous membranes colour, respiration rate and character, pathological noises during breathing act,  intercostal spaces breathing retraction);

–         in the inspiration is difficult or oral cavity is filled with gastric contents, saline or blood provide airways patency (remove foreign bodies or liquids);

–         in case of ineffective respiration begin artificial ventilation;

–         check the pulse over peripheral and central arteries;

–         check photoreaction by raising the eyelids;

–         call for help (actually this is your primary task, but try to use help of witnesses and don’t leave patient alone, especially if you are uncertain about his breathing ability).

 To place patient into “recovery position” you should:

a. place the arm nearest to you at a right angle, flex the opposite knee

b. turn patient aside by pulling the flexed knee and shoulder on the same side; then press the hand of the upper arm to the chick; make sure breathing is not difficult.

 Some comatose patients can be hyperreflexive, hyperkinetic and disposed to cramps.

In case of cramps you should:

–         lay patient in a supine position on a flat surface (to avoid injuries);

–         prevent tongue biting inserting the gag or any available items (like stick or spoon wrapped with cloth);

–         keep the airways open (usual methods described above) and hold the head in order to prevent trauma and asphyxia;

–         provide oxygenation with the mask;

–         between the attacks get an i/v access and give the patient  10-20 ml of 25% magnesium sulphate solution, 2 ml of 0,5% Diazepam solution;

–         clean the oral cavity from blood, saliva, gastric contents;

–         if patient’s breathing is inadequate provide artificial ventilation.

 

            5.3 Diabetic comas.

      Diabetic ketoacidosis.

Diabetic ketoacidosis is a type of hyperglycaemic diabetic coma. It appears in case of diabetes decompensation, which can be caused by inadequate insulinotherapy (wrong dosage), violations of diet (overeating, alcohol abuse), other diseases (usually of infectious etiology – pneumonia for example). Sometimes coma is a first symptom of diabetes.

One more time pay attention to the detailed anamnesis: ask the relatives about the onset of the episode. Did the patient feel unwell few days before decompensation? Was he complaining of weakness, thirst, nausea, vomiting, frequent urination, acetone-like breath odor?

The biochemical foundation of diabetic coma is within the mechanisms of cellular glucose consumption: when cells are not able to absorb glucose it is being accumulated in the blood and thus increases blood osmolarity. Due to osmotic pressure laws fluid will flow from the tissues to the vessels according to the gradients of concentration. This is the mechanism of thirst in case of diabetic patients. When glucose concentration is over10 mmol per liter kidneys fail to reabsorb it completely from the urine and thus it begins to exude with the urine. The water follows glucose according to the already mentioned osmosis rules and this is the reason of diabetic polyuria and dehydration of diabetic patients. Simultaneously cells are suffering from the lack of energy caused by glucose consumption disorders. In order to maintain their vitality cells begin to use other than glucose energetic metabolites: proteins, fatty acids, etc. This ends up with ketosis (accumulation of ketone bodies) and acidosis. Cells begin to loose potassium and this brings hypokalaemia (potassium is not returning from the urine to the blood).

Your clinical and laboratory findings can be next:

–         dehydration symptoms:  body weight loss; dry skin and mucous membranes; decrease of skin turgor, eyeballs tone, blood pressure and central venous pressure, urinary output;

–         metabolic acidosis signs: acetone-like breath odour, Kussmaul breathing (deep noisy breathing), face hyperaemia (acid substances in blood cause dilatation of small vessels and they become overfilled with blood- hyperaemia appears);

–         nausea and vomiting: caused by accumulation of acids within the gastrointestinal tract – increased concentration of acid metabolites in the blood induces compensatory mechanisms of organism protection, among them mucous membranes secretion is one of the most effective;

–         laboratory tests: glucose over 6,6 mmol/, sometimes even more than 30-40 mmol/l; pH is 7,2 and less (uncompensated acidosis); hyperkalemia is caused by cellular potassium lost (with corresponding cellular deficiency of this cation); urine contains ketone bodies; blood tests prove dehydration (hemoconcentration signs: increase of hematocrit, haemoglobin, protein, red blood cells);

First aid: provide general methods of comatose patients treatment – control airways patency, adequacy of ventilation, call for help.

Intensive treatment.

1.         Provide oxygenation with the oxygen mask or nasal catheter. If it is necessary perform the intubation and begin artificial ventilation.

2.         Get an i/v access, insert urinary catheter and gastric probe; if you have enough time take care about the central venous line.

3.         Begin the infusions: saline 1 000 ml during first hour, then 500-1000 ml per hour. Patients with coexistent cardiac diseases should be controlled very carefully: check their central venous pressure and diuresis (should not be less than 40 ml/hour).

4.         Insulinotherapy: initial bolus of 10-20 Units of simple insulin (or 0,2-0,3 U/kg/hour in prolonged infusion); supportive dose is 0,1 U/kg/hour. If in 3-4 hours glucose concentration is not 30 % less dose should be doubled; if in 4-5 hours glucose concentration is not 50% less – dose is doubled again. But the speed of glycemia reduction should not be too high: make sure it is not over 5,5 mmol/l. During first 10 hours don’t try to reduce to the level less than 14 mmol/l. When glucose concentration will reach 14 mmol/l reduce the insulin infusion to 0,05-0,1 U/kg/hour or change the way of insulin admission into subcutaneous injections every 3-4 hours. Usually 5-10 % solutions of glucose are used with insulin infusions to stop pathological fatty acids metabolism.

5.         Control the potassium level according to the blood tests results: in case of hypokalemia add 40 mmols of potassium per each liter of solutions you give i/v, but not faster than 20 mmol/hour.

6.         In case of prolonged treatment use antibiotics for infectious diseases prevention. In case if diabetes was decompensated by infection this will be your aetiological treatment of coma.

7.         Take care about DIC-syndrome prophylactic: 5000 U of heparin s/c under the coagulation tests control or low molecular weight heparins s/c (0,6ml of fraxiparine once a day).

8.         If acid-base disorders are serious (pH<7,1) use 100 ml of 4% sodium bicarbonate solution during first hour and control  acid-base balance.

You can calculate the necessary volume of sodium bicarbonate according to the formula:

VNaHCO₃ (mmol)= 0,3*BE*BW,

BE- base excess (with “-”)

BW – body weight

9.         Symptomatic treatment: if necessary use nootropics, heart medicines and hepatic protectors.

10.    Control vital functions carefully and don’t forget that decompensation of diabetes probably had curable external reason. So your task is to find it and provide proper treatment.

 

Hyperosmolar nonketotic coma.

Hyperosmolar coma is a type of hyperglycaemic coma, caused by high glycemia without ketosis. This complication appears as a consequence of dehydration in elderly patients (in case of diarrhoea, vomiting, burns, excessive perspiration or diuresis). Hyperosmolar coma is diagnosed through the laboratory tests showing plasma hyperosmolality (check chapter 9 for details). If plasma osmolality is over 320 mOsm/l hyperosmolar coma is proved.

Intensive treatment is much alike the therapy of usual hyperglycaemic coma, however rehydration with hypotonic solutions is the main key to success in this situation (use 0,45% saline solution or 2,5% glucose solution).Us usual schemes for insulin therapy and treat the reason of dehydration. Remember: you should never use 4% sodium bicarbonate solution: its osmotic concentration is 3 times higher than the plasma osmotic concentration!

 

Hyperlactacidemic coma

Hyperlactacidemic coma is a diabetic coma, which appears in decompensated diabetic patients who suffer from hypoxia (disorders of respiration or oxygen transportation). In case of oxygen deficiency intracellular respiration is blocked and acid metabolites (including lactic acid) are accumulated. This brings acidosis and diabetic decompensation.

The most common reasons of hypoxia are pneumonia, shocks and anaemia.

Intensive treatment includes usual steps of hyperglycaemia therapy, but main accent is made over the liquidation hypoxia:

–         check the efficiency of respiration and improve it if necessary (mask oxygenation or even artificial ventilation);

–         provide shock treatment if the it is the reason of patient’s comatose condition;

–         transfuse blood components if the cause was anaemia;

–         inhibit excessive metabolic reactions (normalize body temperature, use sedative medicines or neuroleptics if patient has psychomotor excitement and agitation);

–         use antihypoxants (cytochrome c for example).

 

Hypoglycaemic coma

As you can see from the name hypoglycaemic coma is a condition of low glucose concentration in the blood. Unlike most of the previous types of diabetic coma it develops really quickly: within 30-60 minutes. The most common reason for this coma is improper insulin admission or diet violations (insulin overdose or lack of meal after insulin injection). Among the other reasons are: overdose of oral hypoglycaemic drugs (sulfonylurea), physical exercises without insulin dose correction, chronic alcoholism (violated glycogenolysis), hepatic diseases, postoperative gastric diseases (influence speed of glucose absorption).

Your clinical findings will be mostly connected with brain energetic deficiency: weakness, dizziness, coordination violations, dysphoria and inadequate behaviour, unconsciousness and cramps appear as a result of neuroglycopenia (as you remember glucose is the only energetic substrate for neurons, unlike other organs brain is 100% dependable on this monosaccharide).

Hypoglycaemia is classified according to the severity of the symptoms as mild (consciousness preserved, patient is able to take care of himself and hypoglycaemia is liquidated by oral admission of simple carbohydrates), moderate (patient needs help, but his condition is improving after oral admission of simple carbohydrates) and severe (patient is unconscious, needs help and his hypoglycaemia is liquidated only with parenteral glucose infusion).

When glucose concentration is 3,33-2,77 mmol/l you observe only mild hypoglycaemic symptoms. When it diminishes to the level 2,77-1,66 mmol/l the clinical picture is complete (except the unconsciousness). Glucose concentration less than 1, 66 mmol/l  induces coma. Hypoglycaemia lasting 4-6 hours can end up with irreversible cellular damages and even brain death.

Clinical picture is characterized with: pale skin wet from sweat; hemodynamics (central venous pressure, blood pressure) and other systems might be not involved in the initial stages; eyeballs tone and skin turgor are normal, mucous membranes are moist. Breathing is normal, not pathological Kussmaul breathing of ketoacidosis. There is no acetone-like breath odour. Urinary output is normal.

Those clinical features are quite typical, but to prove hypoglycaemia you should wait laboratory results (blood tests will show low glucose concentration).

 

Immediate aid.

In case of mild hypoglycaemia patient should eat 10-20 grams of simple carbohydrates (1-2 slices of bread, 2-4 candies, 200 ml of juice). If glucose level is not normalized within 20 minutes patient should take 10-20 grams of complex carbohydrates (few spoons of cereal for example) to prevent hypoglycaemic ricochet. Moderate hypoglycaemic should be treated simultaneously with simple and complex carbohydrates (10-20 grams of each).

 

Intensive therapy.

In case of severe hypoglycaemia use usual algorithms:

–         provide oxygenation and adequate ventilation;

–         get an i/v access as soon as possible;

–         give 20-40-60-80-100 ml of 40% glucose solution (actually lately it is recommended to use 20% solutions because they cause less irritation of the peripheral veins); the precise dose you will choose according to clinical improvement of CNS condition (but not more than 120 ml);

–         in glucose solutions are not effective prescribe 1 mg of glukagon s/c; 1 ml of 0,1% adrenaline solution s/c, 3060 mg of prednisolone solution i/v;

–         additionally you can use: 100 mg of cocarboxylase i/v, 5 ml of 5% ascorbic acid solution,- or any required symptomatic medicines;

–         in case of brain oedema use 15% mannitol solution (0,5-1,0 g/kg) i/v;

–         even after clinical improvement patients should stay in the ITU for a while, because his condition is still unstable and encephalopathy is still probable.

In children: when you are out of hospital use glukagon subcutaneously (0,5 mg with children under 5 years and 1 mg with elder kids). When you are in the ITU use i/v infusions of 20% glucose (1 ml/kg) during first 3 minutes, then 10% solution of glucose (2-4 ml/kg), check the glycemia and if you will not see the CNS improvement continue with 10-20% solutions of glucose and keep glucose concentration at the level of 7-11 mmol/l. Check glycemia level every half an hour or hour.

 

Control tests.

1.         According to the GCS deep coma is characterized with:

A. 4-5 points

B.13-14 points

C.11-12 points

D. 3 points

E. complete lack of reaction to external stimuli

2. What is the condition of normal CNS functioning?

A.  getting of 20-25 % of circulation blood volume every minute;

B. glycemia level not less than 3 mmol/l;

C. normal concentration of blood proteins and lipids;

D. brain should get at least 10% of total blood oxygen;

E. plasma osmolality should be 185-210 mOsm/l

3. Hyperglycaemic ketoacidotic coma is not characterized with:

A. metabolic acidosis;

B. overhydration;

C. low central venous pressure;

D. respiratory alkalosis;

E. severe paleness.

4. Hypoglycaemic coma is characterized with:

A. critically low blood pressure;

B. decreased tone of eyeballs;

C. wet skin;

D. acute cardiac failure;

E. noisy frequent breathing.

 

Task 1.

Andrew, the doctor, is examining Patience, the patient of 52. Patience is unconscious. His breathing is noisy and frequent; he has acetone-like breath odor; his skin and mucous membranes are dry; his blood pressure is low.

1. What symptoms will help Andrew to make a proper diagnosis?

2. Write the algorithm of Andrew’s actions: clinical examination and laboratory diagnostics.

Task 2.

Choose the symptoms typical for:

a. hyperglycaemic coma;

b. hypoglycaemic coma.

1. Acetone-like breath odour. 2. Paleness.3. Dry skin and mucous membranes. 4. Wet skin.5.  Hyperaemic face. 6. Tachycardia.7. Normal heart rate. 8. Decreased tone of eyeballs.9.Normal eyeballs tone. 10. Usual breathing rate.11. Deep breathing. 12. Normal blood pressure. 13. Hypotension. 14. Normal urine output. 15. Oliguria. 16. Hyperkalemia. 17. Normal potassium concentration. Hypokalemia.19. Increased hematocrit. 20. Unchanged hematocrit. 21. Hyperglycaemia. 22. Hypoglycemia. 23. Central venous pressure over 4 cm H₂O. 24. Central venous pressure 6-10 cm H₂O.

 Task 3. What medicines are not allowed for patients with hyperosmolar nonketotic coma and why?

a. Insulin; b. saline solution; c. 2,5 % glucose solution; d. 4% sodium bicarbonate solution; e. 10% calcium chloride solution; e. 0,45% sodium chloride solution; f. mannitol solution; g. heparin; h. spironolalactone; i. prednisolone.

 Task 4.

Andrew, the student of medicine, is a witness of such situation: in the street man suddenly felt and in few seconds cramps began.

What should Andrew do? What is the probable reason of this situation?

 Task 5.

Patience, the patient of 50, was found unconscious by the ambulance workers at 4 o’clock in the morning. During the admission to the hospital: patient is not reacting to pain stimuli. Respiration is normal, however in supine position airways loose patency. Alcohol odour is quite evident. Pupils are asymmetric, right is wider than the left, photoreaction is inhibited. Haemodynamics is stable. Abdomen is soft, peristalsis is active. Urination is not controlled.

What is the probable diagnosis? What treatment should be prescribed?

 

Acute poisonings.

 

Acute poisoning is a chemical injury, which occurs when chemical substance gets to the organism and violates its vital functions. If the substance is aggressive enough and proper treatment is not provided on time poisoning will bring death.

Although there are over 500 toxic substances which may cause acute poisoning, clinical picture is made up of quite similar syndromes. Proper diagnostics of these syndromes allows avoiding life-threatening complications and gets the chance to make correct preliminary conclusions about the nature of poisoning.

 

8.1 Main clinical syndromes of poisonings.

Affection of central nervous system manifests as excitation or depression of patient’s mental activity. Depression of CNS has different stages: confusion, stupor, spoor and toxic coma. One of the coma’s deepness criteria is reaction of the patient to the painful stimuli (you can also check reaction to smell of ammonium chloride). Lack of reaction is a sign of coma. Don’t live such patient without observation, because his condition is severe and at any moment life-threatening complications may appear: those patients have tendency to bradypnoea up to complete respiratory arrest. Also you should not forget that decreased tone of soft palate and tongue in a supine position will violate patency of the airways and patient can die of asphyxia. In addition comatose condition influences reflexes and lack of swallowing can lead to entrance of saline and gastric contents into the airways (and thus to development of aspiration pneumonia).

Usually CNS depression is caused by excessive alcohol consumption or admission of its surrogates, overdose of neuroleptics, sleeping pills, drugs, sedative medicines, antidepressants and carbon monoxide poisoning.  You can remind intensive treatment of comatose patients in the chapter 5.

Some poisoning are followed with acute intoxication psychosis (mental disorders, hallucinations, time and space disorientation, inadequate behavior). This clinical picture you can observe in case of atropine poisoning (and also atropine-like agents: tincture of dope, henbane, amanita) or cocaine, tubazid, antihistaminic drugs and organophosphates poisoning.

In case of psychosis you will have to immobilize patient in the bed for his own good and safety (to avoid injuries both patient’s and those of the stuff). You will also have to do this in order to maintain i/v lines for antidotes and sedative infusions (aggressive patient will try to remove everything he or she considers irritating). Constantly observe the patient’s vital functions.

 

Toxic affection of the respiratory system can progress as the violation of:

a. external respiration – neurogenic form, aspirations and obstructions of the airways which bring hypoxic hypoxia;

b. hemoglobin’s function – aniline and nitrobenzene create methmoglobin, carbon monoxide connected with hemoglobin creates carboxyhemoglobin and neither the first nor the second is capable of normal oxygen transportation; heavy metal, organic acids and arsenic poisonings  lead to destruction of the red blood cells and emission of the free hemoglobin into the plasma;

c. oxygen transportation due to the decrease of circulating blood volume – exotoxic shock;

d. cellular respiration – tissue hypoxia occurs when cytochromes are blocked with toxins like cyanides.

Practically all severe poisonings earlier or later lead to hypoxia, because they violate oxygen supply, transportation and consumption.

Your immediate therapy actions in this situation will be:

–         to assess of respiratory system (described above);

–         to provide of airways patency (cleaning of the oral cavity, aspiration of the saline and gastric contents, conicotomy if necessary, etc.);

–         to begin oxygen supply (face mask, nasal catheter);

–         to start artificial ventilation if necessary;

–         to prescribe antidotes if they are available (methylene-blue in case of nitro compounds poisonings, unithiolum in case of heavy metals and arsenic poisonings, cytochrome c in case of tissue hypoxia);

–         to start hyperbaric oxygenation in case of carbon monoxide poisoning;

–         to begin infusion therapy in order to stabilize the hemodynamics;

–         to start general detoxification;

–         to prescribe symptomatic treatment and provide prevention of the complications (for example prescription of antibiotics).

 

 

Affection of the cardiovascular system manifests as inability of the heart and vascular bed to provide adequate blood supply of the organs, which leads to metabolic disorders and in the worst case to death. Severe toxic damage of cardiovascular system brings acute cardiovascular failure: primary toxic collapse, exotoxic shock, secondary somatogenic collapse.

Primary toxic collapse appears in case of massive poison admission, when compensatory mechanisms are not quick enough to resist the chemical aggression. Immediately or minutes after poisoning patients begin to suffer from reduced cardiac output and thus from decreased blood flow in the tissues. Peripheral pulse is weak or absent, blood pressure critically lowers and cardiac arrest can appear. In most cases of primary toxic collapse ambulance is not able to save the life of the patient due to the fulminant development of life-threatening complication. However you should remember that such collapse occurs only in 5 % of the cases.

Exotoxic shock is the reason of death for 70 % of poisoning victims. Violations of hemodynamics on one hand are caused by direct heart and vessels damage and on the other hand by compensatory sympathetic and adrenal reactions. On the background of CNS and gastrointestinal system violations you will observe disorders of systemic hemodynamics and microcirculation: arrhythmias, decrease of blood pressure, central venous pressure, cardiac output and diuresis. The peripheral vascular tone changes: toxins induce spasm or dilation of arterioles with the ischemia of one and hyperemia of other tissues. Depending on the body reaction on intensive treatment shock can be compensated, decompensated reversible and decompensated irreversible.

In case of toxic shock you should:

–         get an i/v line (preferably several, including central venous access);

–         start infusions of colloids (albumin, rheopolyglucin, hydroxyethylstarch solutions) and crystalloids (saline, glucose solutions, polarizing solution) in order to normalize blood pressure, heart rate and diuresis; sometimes infusion dose is up to 100-150 ml/kg, (7-10 l/day);

–         constantly control patient’s condition: monitor the heart action, blood pressure and central venous pressure;

–         provide antidote treatment and detoxification; remember that extracorporeal detoxification is possible only after the stabilization of the hemodynamics (systolic blood pressure >90 mm Hg ).

Secondary somatogenic collapse is the reason of death in 25% of the cases. It can occur few days after poisoning, when the toxin is already eliminated from the body, however the tissue changes (in the lungs, liver, kidneys, heart) are irreversible. Necessary treatment: hemodynamics stabilization, improvement of microcirculation, intensive therapy of functional disorders and organic changes (artificial lung ventilation, hemodialysis, cardiac support, etc.).

 

Toxic affection of gastrointestinal tract.

Usually poisoning provokes usual protective reactions: nausea, vomiting, diarrhoea. Chemically aggressive agents can cause “corrosive” effects: concentrated acids and bases can burn the mucous membrane of oral cavity, oesophagus and stomach (vomit is coloured with blood). Profuse vomiting and diarrhoea bring dehydration, electrolytes loss and acid-base imbalance. Especially rapid those complications appear in children.

After recovery patients with chemical burns of gastrointestinal mucous membranes may suffer from cicatrisation and stenosis of digestive tract.

Be aware of the fact, that intensive usage of narcotic pain killers and sleeping pills can lead to inhibition of peristalsis and thus to constipation and slow elimination of toxins.

Immediate aid actions:

–         clean the stomach. If the patient is conscious stimulate vomiting with the pressing on the root of the tongue or with 2-4 liters of slightly salted fluid. Don’t you ever do this in case of chemical burns!

–         if you have the skills and possibility insert the stomach probe and evacuate gastric contents with the help of 10-15 liters of water; if necessary give also antidotes through the probe; you can also use probes with several channels;

–         after the gastric lavage in order to bind toxins use enterosorbents (activated charcoal for example);

–         stimulate stool with saline laxatives (150-200 ml of 33% magnesium sulfate solution) in order to remove connected with the toxin sorbent from the intestines;

–         cleansing enemas also help to eliminate toxins from the body.

 

Toxic affection of liver and kidneys.

This syndrome is caused by primary toxic damage of the liver and kidneys (nephrotoxic and hepatotoxic poisons) or by the secondary disorders of their functions due to violations of blood flow and oxygenation.

Liver is the main detoxification and biotransformation center of the organism, so it takes the “main blow” during intoxication. Intensive detoxification increases metabolic activity and oxygen consumption of the liver several times. Hepatocytes become very sensitive to hypoxia.

Light forms of toxic and hypoxic affections can develop without clinical manifestation. However they will be noticeable in laboratory tests (elevation of transaminases, bilirubin, phosphates). Severe poisoning will bring to toxic hepatitis and even hepatic coma.

Among the hepatotoxic substances are: heavy metals salts, dichloroethane, ethylene glycol, deadly amanita toxins.

To protect the liver you should:

–         eliminate the toxic substance from the gastrointestinal tract;

–         give antidotes if they exist (unithiol for heavy metals salts, lipoic acid for deadly amanita);

–         prescribe cleansing enemas 2-4 times a day (to prevent intoxication with the wastes accumulated in the intestine);

–         use extracorporeal detoxification (hemosorbtion, plasmapheresis, artificial liver);

–         provide adequate oxygenation and blood supply of the liver;

–         prescribe symptomatic treatment.

Kidneys are very important for the elimination of the poisons circulating in the blood. So in many cases they are also the “target” of the toxin.  They can be damaged primary (poison affect their tissues directly) and secondary though the violations of vital functions (for example hemodynamics in case of exotoxic shock). Their condition you can control with the help of urine output per hour, which normally is not less than 0,5 ml/kg.

To prevent the renal failure you should:

–         eliminate the poison as soon as possible (gastric lavage and enemas for gastrointestinal tract; hemodialysis, hemosorbtion, plasmapheresis for blood);

–         give antidotes if they exist (unithiol for heavy metals salts, sodium bicarbonate for hemolytic poisons, ethylic alcohol for ethylene glycol and methanol);

–         treat disorders of hemodynamics (therapy against exotoxic shock);

–         stimulate the urine output with the diuretics on the background of previous rehydration: this will allow you to eliminate diluted in the plasma toxins faster and to prevent renal failure; kidney is an organ which functions normally only if works intense;

Clinical observations tell us, that incredibly massive infusions (10-20-30 l/day) with diuresis stimulation really help patient to dilute and eliminate the toxin without kidneys damage.

In case of acute renal failure you should treat the patient according to the principles described in chapter 6.

 

8.2. Ethylic alcohol poisoning.

This type of poisoning appears in case of excessive alcohol consumption. It is one of the most common poisonings, as well as one of the lightest and prognostically the most favourable (organic damage is rare). However combined with comorbidities and complications it becomes one of the first reasons of death in toxicology, so don’t underestimate it.

Alcohol poisoning, unlike drunkenness, has the characteristic signs of intoxication: vomiting, inhibition of CNS, disorders of cardiovascular system and breathing. Patients usually are in comatose condition. Pay attention to their appearance: clothes are untidy, you caotice sings of involuntary urination or defecation. There is alcohol breathing odour. Skin of the face is hyperaemic and dry. Cyanosis is a sign of respiratory insufficiency, grey shade of skin is a symptom of cardiac disorders. Wet skin might be the symptom of hypoglycaemic coma, hypercapnia or organophosphate poisoning, which are “covered” with the obvious clinic of alcohol poisoning. In case of moderate coma vital functions are usually not involved. Pupils are narrowed or dilated, photoreaction is preserved. Objective criterion of alcohol poisoning is alcohol concentration of the blood:

–         less than 1,5‰ – light inebriation

–         1,5‰-3,5‰ – moderate inebriation

–         3,5‰ and more – severe inebriation

Lethal concentration of alcohol is 5-6‰.

The most common complications of alcohol poisoning are next:

–         obstruction of the airways with the tongue, soft palate or biological fluids (vomit, saline, sputum, blood) in supine position;

–         regurgitation of the gastric contents and development of aspiration pneumonia; lethality is nearly 70%;

–         head traumas with brain injuries: patients usually fell and hurt themselves; the problem with such injuries is that the clinic of hematoma (subdural, epidural, intracerebtal) is quite often “covered” with alcohol intoxication and this is why you should always remember about the differential diagnostics. To make a correct diagnosis in case of coma you should check the specific symptoms such as anisocoria (there is no poisoning which causes pupil’s asymmetry!), signs of head injury (scratches, bruises, skull deformations, oto-liquorrhea and nasal liquorrhea, nasal and ear bleeding), asymmetric tendon reflexes and muscle tone, disparity between the amount of alcohol and deepness of coma, prolonged unconsciousness (alcohol coma even without proper treatment lasts only 3-4 hours);

–         other traumatic injuries (rib fractures which violate external breathing, spleen or liver ruptures with haemorrhagic shock, ruptures of hollow organs with peritonitis; limb fractures);

–         compartment syndrome appears when certain enclosed space within the body for several hours suffers from the decreased blood flow (for example when patients spends few hours in one inconvenient position); even when blood supply will be restored necrotic products will continue pathological process through toxic affection of the life-important organs (for example free myoglobin can cause renal failure).

There is always possibility of chronic diseases exacerbations on the background of alcohol poisoning (stroke, myocardial infarction). Remember about the necessity of complete examination (inspection, palpation, percussion and auscultation of undressed patient) of such alcohol victims – it is the only way to find all the “diagnostic mysteries” patients hide!

Intensive treatment:

–         evaluate CNS condition (deepness of the coma);

–         provide airways patency and adequate respiration (described above; if necessary – intubate the patient and begin artificial ventilation);

–         check the cardiovascular system: heart rate, pulse, blood pressure;

–         in case of severe hemodynamic disorders provide infusion therapy;

–         insert the stomach probe and remove its contents using lavage with water;

–         take blood samples and check blood alcohol level (obligatory!);

–         prescribe intravenously:  60-80 ml of 40% glucose solution, 60-80 ml of 4% sodium bicarbonate solution, 5-10 ml of 5% ascorbic acid, 1-2 ml of vitamin B₁ solution;

–         if there are no comorbidities add analeptic solutions i/m (2-3  ml of caffeine or 2 ml of cordiamin);

–         in case of severe intoxication begin forced diuresis.

 

8.3 Poisonings with alcohol surrogates.

Patients can be poisoned with: home-distilled vodka, Cologne water, denatured alcohol, methyl alcohol, lotion, brake fluid, etc. The peculiarity of such poisonings is complex effect of the alcohol and other toxic components of the “drink”.

The most toxic are methyl alcohol and antifreeze (ethylene glycol) – their lethal dose is 60-100 ml. Lower doses cause neuritis of optical nerve and thus blindness (methyl alcohol), acute renal and liver failures (ethylene glycol).

In case of these poisonings detailed anamnesis and blood identification of the poison (gas chromatography) play the most significant role in the diagnostics. However for the prognosis volume of the poisonous fluid, duration of its influence, functional condition of the liver and effectiveness of the antidote therapy and detoxification are the most important.

In the body methanol and ethylene glycol are metabolised according to so called “lethal-synthesis”: during the breakdown of the poison in the liver there are created substances much more toxic than the parent compounds.

Intensive therapy:

1.         Gastric lavage with potassium permanganate (oxidizes methyl alcohol).

2.         Give antidote:  50 ml of 40% ethylic alcohol solution every 3 hours orally or 100 ml of 5% ethanol solution intravenously slowly combined with glucose solution during 2 days. Antidote will block the process of their biotransformation in the liver until the poisons will not be eliminated from the body.

3.         Actively eliminate the poison from the body through repeated gastric lavages, forced diarrhoea, extracorporeal methods of detoxification (hemodialysis, hemosorbtion, plasmapheresis).

4.         In order to treat optic neuritis you should perform retrobulbar inject of steroids.

5.         Symptomatic treatment.

 

 

8.4 Drug poisonings.

In civilized countries these poisoning are the main reason (65-70% of cases) of hospitalization in toxicology units. Usually patients overdose sleeping pills, narcotic painkillers, antihistamine drugs, hypotensive medicines. Among the reasons are suicide tries, drug abuse, toxicomania and accidental overdose due to hectic pace of modern life, etc.

Clinical picture is usually connected with CNS affection. There are phases of somnolence, sleep and coma. Depending on involvement of other systems coma can be complicated or uncomplicated. Usually respiratory complications appear: inspiration centre depression, violations of airways patency due to soft tissues (tongue, soft palate) or biologic fluids (blood, sputum, saline), pneumonia. In 15-20% of cases the poisoning development is complicated with the exotoxic shock. The peculiarities of this shock are next: circulatory disorders with blood stagnation in the pulmonary circuit, toxic affection of the myocardium and decrease of energy metabolism of the organism.

To indicate the poison you should ask relatives and witnesses and check things of the patient (for example you can find medicine packages). Evaluate the size of the pupils: extremely narrowed pupils (“poppy seeds”) are the effect of narcotics admission; narrowed pupils might be the sign of sleeping or sedative medicines overdose; dilated pupils are the symptom of clofelin, antidepressants or neuroleptics administration; wide pupils covering the whole iris are usually the sign of atropine poisoning (or a poisoning with atropine-like substances: dope, henbane, amanita).

Principles of the intensive treatment in the toxicology unit:

–         clean the gastrointestinal tract as soon as possible (gastric and intestinal lavage, enterosorbtion, cleansing enemas) and as often as necessary;

–         provide adequate respiration (check airways patency);

–         in case of comatose patients intubate the trachea and begin artificial ventilation (sometimes it is necessary for weeks);

–         control hemodynamics and treat its violations (infusion therapy and adrenergic agonists or antagonists if necessary);

–         stimulate diuresis: patients with barbiturate poisoning should be treated with alkaline forced diuresis in order to eliminate the toxin (add to the infusion 400-600 ml of 4% sodium bicarbonate solution and prescribe diuretics);

–         use antidotes: naloxone for opiates, pharmacological antagonists for anticholinergic and cholinomimetic agents; don’t you ever prescribe central analeptics for comatose patients with drugs poisoning – cordiamin, caffeine, bemegride , cytiton, lobelinum can cause “cerebral blood flow steeling effect” and thus they deepen the hypoxia of brain cells!

–         provide extracorporeal detoxification to eliminate toxins (hemodialysis, hemosorbtion, plasmapheresis);

–         prescribe antibiotics for infectious diseases prevention (for example in case of prolonged artificial ventilation);

–         symptomatic treatment.

 

8.5 Alkali and acid poisonings.

These poisonings are among the most severe and difficult to treat. Accidentally or intentionally (suicide) victim can take mineral acids (hydrochloric, sulphuric, nitric acids), organic acids (acetic or oxalic acid), alkali (ammonium chloride, battery fluid, etc.).

When corrosive substance gets into the body along its way inside chemical burn appears: mucous membranes of oral cavity, throat, oesophagus, stomach are injured. Together they make nearly 14-15% of the body surface. Patients suffer from unbearable pain, eating and drinking are disabled. In case of acid burn coagulatioecrosis appears; alkali burn is more severe, because colliquative necrosis penetrates deeper into the tissues ruining the vessels and causing bleedings. Organic acids easily get into the blood. Sometimes chemical substances or their vapours also get into the airways and thus oedema and risk of asphyxia appear.

Usually part of aggressive substance is spilled over the chin and you caotice the burn. Systemic disorders are characterized with exotoxic shock which develops as burn shock (unbearable pain, dehydration, toxic affection of the heart, decrease of cardiac output, spasm of arterioles and microcirculation block). Organic acids also provoke hemolysis of red blood cells: free haemoglobin transforms into hydrochloric haematin and obturates renal tubules, causing acute renal failure.

Intensive treatment principles:

–         evaluate patient’s condition: external respiration, consciousness, cardiovascular system;

–         adequate pain relief with narcotic painkillers and non-steroidal anti-inflammatory drugs (1-2 ml of 1% morphine solution; 2 ml of 50% analgin solution);

–         liquidate the spasm of gastric cardia and oesophagus (1 ml of 0,1% atropine solution i/m, 5 ml of baralgin solution);

–         clean the stomach during first 10 hours after poisoning; insert the stomach probe (cover it thickly with Vaseline and don’t push too hard); use water for lavage and don’t try to perform chemical inactivation of the poison, because during the reaction carbon dioxide can exude and acute expansion of the stomach leads to it rupture;

–         provide treatment of shock (sometimes up to 10-12 liters/day of infusions);

–         in case of organic acids poisonings (acetic acid, oxalic acid get into the blood) give 1500-2000 of 4% sodium bicarbonate solution intravenously slowly with diuretics; these actions will help to remove hemoglobin (released due to red blood cells hemolysis) and thus to prevent acute renal failure;

–         in case of obstructive breathing disorders (mucous membrane edema) use steroids (90-120 mg of prednisolone), antihistamine drugs (2 ml of 1% dimedrol solution intravenously), sedative medicines (2 ml of 0,5% diazepam solution); perform tracheostomy or conicotomy if necessary;

–         prescribe antibiotics for infectious diseases prevention (for example in case of prolonged artificial ventilation);

–         symptomatic treatment.

During the recovering period patient may need surgeries for restoration of gastrointestinal tract: the most common practice is the bouginage of the oesophagus or, if necessary, oesophagus plastic.

 

8.6. Poisonings with toxic gases.

 

Among the toxic gases are carbon monoxide, car exhausts, propane and butane, ammoniac gases. The last one is the most toxic: few inhales are enough to cause unconsciousness.

The foundation of the pathology lies within the atypical haemoglobin – carboxyhemoglobin – combination of normal haemoglobin and toxic gas. Oxygen transportation if violated (in case of severe poisonings there are nearly 70-80% of changed haemoglobin) and thus haemic hypoxia appears. In addition within the tissues cytochromes are connected with toxic substances and this leads to tissue hypoxia.

Clinical findings in case of carbon monoxide poisoning depend on the severity of the poisoning. In case of mild intoxication they are: headache, nausea, vomiting. Moderate intoxication shows unconsciousness for 12-16 hours and severe intoxication is characterized with coma, central disorders of breathing, toxic affection of heart and other organs, etc.

If intoxication advances changes of central nervous system become irreversible (brain death is possible).

Intensive treatment.

In case of mild and moderate poisonings you should you should carry the patient out of the toxic atmosphere as soon as possible. In hospital conditions you should provide oxygen supply, get an intravenous line for crystalloids infusion and prescribe vitamins.

In case of severe intoxication begin artificial ventilation with high oxygen flow. Luckily there is an antidote for carbon monoxide poisoning: hyperbaric oxygenation. Connection with oxygen is more natural for haemoglobin and when the pressure of oxygen is higher than its usual partial pressure carbon monoxide is replaced from the haemoglobin. Usually in case of comatose patients 40-50 minutes sessions every 6-12 hours are enough.

To normalize tissue metabolism prescribe antihypoxants: 20% solution of sodium oxybutirate (20-40 mg/kg i/v) and cytochrome c (2-3 ml i/v) every 4-6 hours. To improve microcirculation dilute the blood with crystalloid infusions (check the level of hemodilution with hematocrit – stop when it will reach 0,3-0,35 l/l).

Prevent the infectious complications and brain oedema with standard methods.

 

8.7 Organophosphate poisonings.

These are the poisonings with insecticides, acaricides, herbicides, fungicides, rodenticides, desiccants, defoliants and with chemical warfare agents such as sorin, soman, V-x.

Organophosphate substances are fats and water soluble and thus they penetrate easily through the skin and mucous membranes (gastrointestinal tract, airways, etc.). In the blood they block an enzyme – cholinesterase – responsible for the breakdown of acetylcholine. As you remember acetylcholine is a universal synaptic mediator of nervous impulses and thus its accumulation on the post-synaptic membranes will cause continuous stimulation of vegetative nervous system and cross-striated muscles.

Clinically you will see: nausea, vomiting, cramps; unconsciousness in severe cases. Sometimes in the place of penetration you can see muscle fasciculation (if the poison was administered orally – tongue twitching). Stimulated parasympathetic nervous system shows wet skin, increased salivation and bronchial secretion (sometimes you can even see white phlegm in the mouth – don’t mistake it with the pink phlegm of pulmonary oedema), narrowed pupils, bradycardia (heart rate 40-30 beats per minute). In addition to the obvious clinic you can always check the environment of the patient for the signs of organophosphate poisons (specific smell, containers with toxins, etc.).

One third of patients suffer from exotoxic shock, which primary causes hypertension and then hypotension, unconsciousness and depression of respiration.

Immediate aid:

–     take patient out of the dangerous environment (if you suspect that the mechanism of poisoning is inhalation);

–         clean the stomach with large amounts of cold water; repeat it several times, because these substances are excreted through the mucous membranes of gastrointestinal tract;

–         give saline laxative;

–         if the poison affected skin – wash it with alkaline solution.

Antidotes:

a.          use peripheral m-anticholinergic drug – atropine: during the first few hours 2-3 ml of 0,1% atropine solution (up to 30-35 ml during the whole period of intensive atropinization); pay attention to the signs of atropine administration as they are the measure of your antidote treatment effectiveness: termination of excessive bronchial secretion, dilation of the pupils, tachycardia (90-110/min). During next 3-5 days continue atropine prescription (from 10-15 mg to 100-150 mg/day – period of supportive atropinization). Control clinically the level of atropinization.

b.         use cholinesterase reactivators: 1-2 ml of 15% dipiroxim solution i/m, up to 600 mg; 3 ml of 40% izonotrozin solution i/m up to 3-4 grams. However remember, that cholinesterase reactivators can be used only 24 hours after poisoning. Later administered reactivators will ne not only ineffective, but also toxic for the patient.

You should also provide usual treatment as soon as possible: infusion therapy, forced diuresis, hemosorbtion, plasmapheresis, hemodialysis and antibiotics for infection preventions.

In case of ineffective external respiration and comatose patient’s condition intubate the patient and start artificial respiration. Convulsions in case of organophosphate poisoning are treated with sodium oxybate (75-100 mg/kg i/v every 4 hours). Cardiac glycosides, calcium chloride, euphillinum are forbidden in case of organophosphate poisonings, because they induce toxic heart affection.

Be aware of the possibility of “second poisoning wave”: even 4-8 days after the stabilization of the patient’s condition clinical picture of the poisoning might return and this time hemodynamics will decompensate quickly.

 

8.8 Mushroom poisoning.

There are edible, non-edible and relatively edible mushrooms. Non-edible or poisonous mushrooms can contain toxins harmful for central nervous system, liver, kidneys and gastrointestinal tract (according to A. Lokay, 1 968). The most dangerous poisoning is caused by deadly amanita. The poison of this mushroom – amanitotoxin- is not destroyed during cooking and there is no way to detect it in usual conditions. In case of severe poisoning the lethality is 80%.

Specific feature of amanita poisoning is prolonged latent period. Sometimes 6-12 hours pass before the first symptoms of the poisoning appear. All the other relatively edible mushrooms reveal clinical signs of the poisoning much earlier – 1-2 hours after consumption.

After the latent period is over on the background of complete health nausea, profuse vomiting and diarrhoea appear. Those symptoms begin second phase of the poisoning – gastroenterocolitic phase. Liver enlarges; patients suffer from pain in the right subcostal area, weakness, and consciousness disorders. Stool becomes watery and contains mucous. Patients loose up to 4 liters of the fluid during the day. Unlike bacterial food poisonings, mushroom poisonings are not characterized with high fever.

Liver failure and acute kidneys injury are the third phase of the poisoning, which begins on the second or third day of disease. Those failures are characterized with hepatic encephalopathy, jaundice, gastrointestinal bleedings, hepatic breath odour and oligoanuria. The level of alanine and aspartate aminotransferases is very high. When liver returns to its usual size and consciousness is changed into coma hepatargia is stated and prognosis for the disease becomes rather unfavourable.

The forth stage is a stage of recovery and is characterized with gradual regression of the clinical picture and normalization of the laboratory results during several weeks. However survival is possible only for those patients, who ate small amounts of the poisonous mushroom.

Knowing about the high lethality and severity of the amanita poisoning prevention methods become very important. Mushroomers should know the difference between deadly amanita and other mushrooms: deadly amanita is a gill-bearing mushroom with olive or green cap. Its gills white are not connected with the stem. Stem has a bulbus with white volva from one side and a white annulus from another side, under the cap.

 

Patients should be treated in a special toxicology units or intensive treatment unit. General principles of intensive therapy are:

–         gastric and intestinal lavage, enterosorbtion and saline laxatives;

–         infusion therapy (necessary to liquidate electrolyte deficiency and provide forced diuresis);

–         support of the liver functioning with lipoic or thioctic acid (1000-2000 mg/day), concentrated glucose solutions, steroids (up to 40 mg of dexamethasone per day) and silibin (50 mg/day);

–         extracorporeal detoxification (hemodialysis, hemosorbtion, plasmapheresis, artificial spleen or liver) as soon as possible;

–         antibiotics if necessary (penicillin); vitamins (B,C,E);

–         external drainage of thoracic duct (decreases intoxication through elimination of toxic lymph).

 

 

8.9 Medical operations and manipulations.

Gastric lavage

Indications: necessity to remove poisons or toxins from the stomach, to clean it before operation or to liquidate stagnation during period after the operation.

Equipment required: gastric probe (with two channels if possible), Janet syringe, water for lavage (15-20 liters of room temperature water), gloves and watertight apron.

Procedure: gastric lavage of comatose patients is a procedure for doctors. In our country nurses are not allowed to do this without control of the doctor: unconscious patients have inhibited reflexes and thus probe can be easily inserted into the trachea instead of oesophagus. In this situation neither cyanosis nor cough may not appear and everything looks just fine, however feeding or lavage try can end with fatal complications (asphyxia and death).

Put on the gloves, choose the probe of necessary size and oil it with Vaseline. Patient should lie on the left side (ask nurse to hold patient’s arms to limit his movements during this unpleasant procedure).

If patient is conscious you can previously use lidocaine spray to anaesthetize mucous membranes. Probe can be inserted through the nose (of course in this case size of the probe is limited) or through the mouse. Don’t push too hard, especially when you are using nasal passage: you can cause bleeding. Ask patient to bow his head to the chest – this will increases chances of correct probe insertion (oesophagus, not trachea). The length of probe you insert can be measured in advance as a distance between earlobe, nose and xiphoid.

Confirmations of correct probe placement:

–         auscultate the epigastrium and simultaneously infuse some air with the syringe- you will hear typical “bubble” noises;

–         if you made a mistake and probe is in the trachea you caotice air released from the distant end of the tube according to the respiratory movements.

  One-time water doe is nearly 200 ml: it will flow out when you will lower the probe or you will have to evacuate the water with the syringe. Repeat these actions until the water wash out the stomach will be clean (usually it takes nearly 10 liters of water).

 

Forced diuresis.

Indications: intoxications of different origin (poisonings, infectious diseases, endogenous intoxications).

Medicines required: normal saline (3-5 liters); detoxification solutions; polarizing solution (400 ml of 10% glucose solution, 10 ml of 7,5% potassium chloride solution, 12 units of insulin), osmotic diuretics ( mannitol in the dose 1 g/kg), furosemid solution (40-80 mg)

Procedure: get and i/v line (central or peripheral) and insert urinary catheter. During the first phase of forced diuresis “water” the patient with crystalloids and detoxification solutions (30-40 ml/kg). During the second phase infuse osmotic diuretics and furosemide solution. Excessive urine output brings potassium loss, which you should treat with polarizing solution. Balance the speed of infusion with the speed of diuresis: generally per 5-7 liters of infused solutions you should receive at least 5 liters of urine.

Constantly control hemodynamics and blood electrolytes.

 

Control tests.

1. What medicine should be used as an antidote in case of severe soporific drugs poisoning?

A. bemegride

B. cordiamin

C. there is no such meidicine

D. unithiol

E. cytiton

2. What is the most common death reason in case of alcohol poisoning?

A. acute liver failure

B. acute respiratory failure

C. acute renal failure

D. acute heart insufficiency

E. collapse

3. What is necessary for the patient, who took 60 ml of acetic essence?

A. to give 4% sodium bicarbonate solution i/v

B. to clean the stomach with alkaline solution in order to neutralize the acid

C. to use unithiol as an antidote

D. to stimulate intestinal cleansing with saline laxatives

E. central analeptics

4. What is the symptom of organophosphate poisoning?

A. pale and dry skin

B. maximal pupil’s dilation

C. tachycardia

D. muscle fasciculation

E. acute liver failure

5. What is used as an antidote in case of severe carbon monoxide poisoning?

A. cytochrome c

B. cordiamin solution

C. unithiol

D. prednisolone

E. antidotes are not used

6. What is typical for deadly amanita poisonings?

A. first symptoms appear in2-3 hours after mushroom meal;

B. low-grade fever

C. latent period of 6-12 hours

D. first symptoms are haemostatic disorders (bleeding)

E. early unconsciousness

7.  What is the necessary aid in case of narcotic painkillers overdose?

A. artificial ventilation

B. cordiamin

C. oxygen supply

D. immobilization of the patient in order to avoid self-injuries during the excitement-phase;

E. cardiac medicines

 

Task 1.

Patience, the patient of 19 is transported to the ITU by witnesses from the street. Clinical findings: unconscious, cyanotic wet skin, 6 breathes per minute, respiration shallow, blood pressure 70/40 mm Hg, heart rate 112/minute. Name the reason of vital disorder and write the principles of intensive care (algorithm).

Task 2.

Patience, the patient of 19, was found unconscious in his own apartment by the ambulance workers. Clinical findings: total cyanosis, shallow breathing, respiration rate 5/min, pupils extremely narrowed, photoreaction is absent, blood pressure 80/40 mm Hg.  In the elbow area there are noticeable signs of injections. Name the reason of vital disorder and write the principles of intensive care (algorithm).

Task 3.

Patience, the patient of 23 was hospitalized into ITU with the diagnosis: mushroom poisoning. It turned out, that yesterday she was eating cooked champignons. 8 hours later she noticed vomiting and diarrhoea. Clinical findings: scleral icterus, dry coated white tongue; painful abdomen (epigastrium and right hypogastric area), painful and enlarged liver (2 cm); hemodynamics and respiration are not violated.

Write the diagnosis and the phase of the disease.

Task 4.

Patience, the patient of 18, is transported to the toxicology unit with delirium. Clinical findings: hyperaemic face, dry skin, dilated pupils. Blood pressure 140/70 mm Hg, heart rate 127/minute. It is know, that 2 hours ago she took 10 unknown tablets during the suicidal attempt. What is the diagnosis and what are your actions?

Task 5.

Patience, the patient of middle age, was found by the ambulance workers in his own kitchen unconscious. Clinical findings: specific smell of organophosphates in the room, signs of vomit on the clothes, miosis,  cold clammy skin with cyanotic shade, foamy white sputum in the mouth, blood pressure 90/50 mm Hg, heart rate 54/minute. What is the diagnosis? What immediate aid should be provided during pre-hospital stage?

Task 6.

Adams family were celebrating the New Year Eve near the fireplace. In the morning came the carol singers and found hosts in a condition of deep sleep.  “Dream team”, the ambulance workers, who came to the place of the accident, stated: 2 adults and their children in comatose condition, vomit signs on the clothes, rapid breathing, pupils dilated with weak photoreaction; heart rate is 110-120 per minute, rhythmic; blood pressure is high.

Name the reason of the accident and describe the actions of the “Dream team’.

Task 7.

Name the poisoning agent for each antidote: a. atropine, b. unithiol, c. naloxone, d.tetacinum, e. ethylic alcohol, f. dipiroximum, g. lipoic acid?

 

Student should repeat next questions

 

Among the natural vasoconstrictors (agents, which cause constriction of the blood vessel) are epinephrine, norepinephrine, serotonin, angiotensin II. Stress enhances the secretion of cathecholamines, their blood concentration increases and arterioles constrict. Spasm of the arterioles is the basis of blood flow centralization: peripheral flow is disregarded in order to provide brain with the oxygenated blood as long as possible. To the group of vasodilatators (agents, which provide dilatation of the vessels) belong “acid” metabolites (lactate, pyruvate, adenylic acid, inosinic acid), bradykinin, acetylcholine, different medicines (neuroleptics, α-adrenergic antagonists, peripheral vasodilatators, ganglionic blocking agents, etc.), some exogenous poisons. All of them cause blood flow decentralization: opening of arterioles and distribution of the blood from central vessels to the capillary bed.

Capillaries are the interweaving network of the smallest body vessels with the general length of 90-100 thousands of kilometers. However simultaneously work only 20-25% of them. They provide metabolic exchange bringing oxygen and nutrients to the tissues and take back wastes of metabolism. Periodically, every 30-40 seconds one of them get closed and others open (vasomotion effect). Capillaries contain 12% of the whole circulating blood volume, but different pathological conditions can increase this amount even 3 and more times.

“Used” blood from the capillaries flows to the venous system. Veins are the blood reservoir, which contains 70% of the total circulating blood volume. Unlike arteries they are capable of volume control and thus they influence the amount of blood, which returns to the heart.

The most important haemodynamic index of venous system is central venous pressure. CVP represents the pressure which blood causes to the walls of cava veins and right atrium. This parameter is an integral index of circulating blood volume, systemic vascular resistance and pump function of the heart. It can be measure with a special device called “phlebotonometer” (pic. 4.9) or with a usual infusion set and a ruler. Normally CVP measured from the sternum point is 0-14 cm H₂O and from midaxillary line is 8-15 cm H₂O.

Central venous pressure decreases (sometimes even to negative) in case of:

– blood loss

– excessive water loss (dehydration)

– distributive shock (decrease of peripheral resistance due to venous and arterial dilatation)

In those conditions decreases volume of blood returning to the heart and thus suffers cardiac output. In case of negative CVP cardiac arrest is highly probable.

Central venous pressure increases in case of:

– heart failure (insufficiency of left or right ventricle)

 – hypervolemia (excessive blood infusion, improper infusion therapy)

 – obstructions to blood flow (pulmonary embolism, cardiac tamponade, etc.)

When CVP over 15-16 cm H₂O is combined with left ventricle insufficiency the risk of pulmonary edema is very high.

 

Blood pressure is an integral index of arterial part of systemic haemodynamics. Talking about blood pressure we may refer to systolic, diastolic, pulse and mean arterial pressure. Systolic (P_syst) and diastolic (P _diast) pressures are measured with the manometer (method with the usage of phonendoscope was invented by M. Korotkoff). Pulse pressure (PP) is a difference between systolic and diastolic blood pressure.

Mean arterial pressure (MAP) is calculated according to the formula:

MAP= P _dias + 1/3 PP                            mm Hg

 

MAP defines the level of pressure necessary for the metabolic exchange in the tissues. Its measurement allows the evaluation of tissue perfusion level.

Blood pressure depends on different factors, but the most important are cardiac output and vascular resistance (mostly arterioles). This dependence is direct, thus you can increase blood pressure using:

–         infusion of vasoconstrictors – solutions of epinephrine, phenylephrine (mesaton), etc. (they will increase the vascular resistance);

–         infusion of hydroxyethyl starch solutions or saline (they will increase circulating blood volume)

–         infusion of cardiac glycosides or other medicine which stimulate myocardium

 

General volume of blood in the body of a healthy adult is nearly 7% from the body weight: 70 ml per kilogram for male and 65 mil per kilogram of body weight for female. Of course circulating blood volume is lower, because part of blood is out of metabolic processes as a reserve. CBV can be measured with the infusion of coloring substance to the blood flow (Evans blue, polyglucin) and later evaluation of its dissolution degree.

Therefore measurement of CVP, BP, cardiac output and circulating blood volume allow to evaluate condition of circulation system of the patients and to provide adequate correction.

 

4.2 Acute heart failure; shock and collapse.

Acute cardiovascular failure is a state of cardiac and vascular inability to provide adequate supply of tissue metabolic needs with oxygenated blood and nutrients. This, earlier or later, causes cellular death.

 

The reasons of the failure vary greatly: mechanic injuries, blood loss, burns, dehydration, exogenous and endogenous intoxications, immediate hypersensitivity reaction, ischemic heart disease, neural and humoral regulation disorders of vascular tone.

Acute cardiac failure is a disorder of heart pumping action. It develops due to primary heart problems or secondary, under the influence of extracardiac factors such as infection or intoxication. There are two types of heart failure: left-sided and right-sided.

 

Left-sided heart failure is an inability of left ventricle to pump blood from the pulmonary circuit to the systemic circuit. The most common reasons of it are myocardial infarction, mitral insufficiency, left AV valve stenosis, aortic valve stenosis, aortal insufficiency, hypertonic disease, coronary sclerosis, acute pneumonia.

Coronary circulation is possible only during the diastole and in those conditions every violation of coronary passability decreases cardiac output. This way during the systole part of the blood is not injected into aorta, but stays in the left ventricle. Diastolic pressure in the left ventricle increases and blood is literally forced to stagnate in the left atrium. At the same time right ventricle functions normally and continues to pump usual amounts of blood to the pulmonary circuit. Thus hydrostatic pressure in the vessels of pulmonary circulation increases, fluid part of the blood moves first to the lung tissue and then, through alveolar-capillary membrane, to the alveolar lumen.

Clinically pulmonary edema begins with dyspnea (during physical activity or rest). Later attacks of dyspnea are connected with persistent cough with white or pink blood-tinged phlegm. During the attack patient tries to sit as in this position breathing is easier. This condition is called “heart asthma”. When hydrostatic pressure is over 150-200 mm Hg, fluid part of blood moves to the alveolar lumen causing development of pulmonary edema.

Pulmonary edema is divided into interstitial and alveolar edema.

Interstitial edema is a condition during which serous part of stagnated in the pulmonary circuit blood infiltrates the lung tissue, including peribronchial and perivascular spaces.

During alveolar edema not only the plasma, but also blood components (red and white blood cells, platelets) get out from the vessels. During the respiratory act blood mixes with the air creating large amount of “foam”, which violates gas exchange. This way, in addition to circulatory hypoxia, hypoxic hypoxia appears.

Condition of the patient gets worth quickly. Sitting position is optimal, but not as helping as previously. Respiratory rate is nearly 30-35 breathes per minute, but attacks of breathlessness are constant. Skin is pale with acrocyanosis. Hypoxia of central nervous system usually causes psychomotor agitation. Respiratory acts are noisy; during cough pink blood-tinged phlegm is released. Auscultation allows you to hear different wet rales, sometimes it’s even possible to hear them standing aside the patient without phonendoscope.

Pulmonary edema can be also divided according to the blood pressure level: the one with elevated pressure is caused by a hypertonic disease, aorta valve insufficiency or disorders of cerebral perfusion; another one is caused by total myocardial infarction, acute inflammation of myocardial muscle, terminal valve defects,severe pneumonia and is characterized with normal or low blood pressure.

Immediate aid

–         make sure patient is sitting with his legs down (orthopnea)

–         provide oxygenation through nasal catheter (before placing oil it with glycerin, insert it to the depth of 10-12 cm – distance from the wing of the nose to auricle) or face mask. Do not use Vaseline, because it can burn in atmosphere with high concentration of oxygen.

However if catheter is not deep enough patient will suffer from an unpleasant “burning” feeling, because oxygen flow will dry mucosa layer of the nasal cavity; also in this situation concentration of oxygen will be lower than expected.

–         put venous tourniquets on the limbs in order to reduce amount of blood returning to heart: venous bed of limbs can reserve up to 1,7 liters of blood;

–         constantly control heart and kidney activity (ECG, SaO₂ , and blood pressure are checked automatically trough the monitor; to control diuresis you should insert Foley catheter;

–         catheterize central vein, because amount of infusions should be based on central venous pressure;

–         use  medical “defoamers” if they are available (ethyl alcohol or antiphomsylan solution) combined with oxygen inhalation

Scheme of oxygenation set connected to “defoamer” container

a.          oxygen source (cylinder with oxygen)

b.         tube with numerous holes sunk into container with defoamer

c.          tube for humidified oxygen (its opening should be over the level of fluid);

d.         patient

 

–         medical treatment: 1% morphine solution (decreases intravascular pressure of pulmonary circuit, inhibits respiration center in medulla oblongata preventive dyspnea progress, sedates patient);

–         solutions of diuretics are used to decrease the circulating blood volume ( 6-12 ml of 1% furosemid solution, solution of ethacrynic acid), however be careful with them in case of low blood pressure; diuretic effect will last up to 3 hours after i/v infusion, the expected diuresis is 2-3 liters

–         if blood pressure allows you can try to use nitroglycerin to reduce intravascular pressure of pulmonary circuit (1 or 2 tablets with 10 minutes interval)

–          cardiac glycosides for improvement of heart action (0,025% digoxin solution, 0,05% strophanthin solution, 0,06% corglicon solution);

–         in case of high pressure (over 150 mm Hg) use ganglionic blocking agents (1 ml of 5% pentamin solution diluted in 150 ml of saline, give i/v slowly; diluted with saline 250 mg of trimethaphan solution), because they reduce pressure in pulmonary circuit and lower the amount of blood getting to right half of the heart, however be careful with the dosage and monitor blood pressure level carefully;

–         never use osmotic diuretics in case of pulmonary edema – they will increase blood volume and thus heart load!!!

–         when everything listed above failed and patient is worsening with every second you should intubate him and start artificial ventilation with positive end expiratory pressure (begin with 4-6 cm H₂O)

 

 

Right-sided heart failure is an inability of right ventricular to pump blood from systemic circuit to the pulmonary circuit due to its weakness or an obstruction to the blood flow.

It occurs in case of pulmonary embolism, right ventricular infarction, excessive infusion therapy (especially including citrated blood) for patients with heart insufficiency, lung diseases (bronchial asthma, emphysema, pneumosclerosis) which cause increase of right ventricular load.

Patients have acrocyanosis, tachycardia, dyspnea, pronounced neck veins, ankle swelling, enlarged liver, ascytis. Central venous pressure is highly increased (up to 20-25 cm H₂O), however pulmonary edema does not appear.

Intensive treatment is mostly pathogenetic:

–         limit the infusions (give only life-necessary solutions, check the water balance of the patient and reduce drinking water if necessary);

–         in case of citrated blood transfusions use 5-10 ml of 10% calcium gluconate solution per every 500 ml of blood to prevent hypocalcaemia;

–         in case of bronchial spasm use bronchial spasmolytics;

–         to remove excessive fluid from the body use diuretics (furosemide solution for example);

–         metabolic acidosis is corrected with 4% solution of sodium bicarbonate (i/v slowly with acid-base state control);

–         in case of pulmonary embolism anticoagulants are used – fraxiparine 0,6 mg subcutaneously; heparin solution – 5000 IU every 4 hours; fibrinolytic drugs (streptokinase, fibrinolysin, urokinase, etc.)

 

Shock is a pathological state which can be described as a tissue hypoxia caused by hypoperfusion. Pathogenetic basis of shock depends on its reason (trauma, toxins, thermal injury) and at the same time on reactivity of the organism (level of defense mechanisms mobilization).

Stimulation of sympathetic nervous system – production of catecholamines and other vasoactive substances by hypothalamus and adrenal glands are the universal response of the body to the stress. Those mediators interact with the receptors of peripheral vessels causing their constriction and at the same time they dilatate the vascular bed of life-important organs. This is so called “centralization of the flow”: rational decrease of blood flow in less important tissues (skin, organs of abdominal cavity, kidneys) in case of aggressive external influence for protecting life itself (brain, heart, lungs).

However influence of shock agents (pain, hypovolemia, destroyed cells, toxic metabolites), extended microcirculation violations (vascular spasm, microthrombosis and sludge) and caused by them tissue ischemia lead to hypoxic affection and cellular death of the internal organs. Further it can bring multiple organ dysfunction syndrome.

 

Collapse is a vascular failure. It occurs when body is not able to provide blood flow according to the new level of its needs (either because reaction is not fast enough or because sympathetic activation fails).Vascular bed volume and circulating blood volume are disproportional: too much blood gets to the microcirculation vascular reserve and the amount, which returns to the heart is not enough for the systemic needs (so called “decentralization” of the blood flow). Cardiac output and blood pressure decrease, that causes hypoperfusion of the central nervous system and thus unconsciousness and life-threatening complications.

Collapse definition is a bit nominal, because if such reaction extends in time the state of shock develops. Shock itself can equally run as a vascular failure or as a sudden clinical death.

 

Pathogenetic classification of shock (according to P. Marino, 1998):

–         hypovolemic

–         cardiogenic

–         distributive

–         mixed (two and more factors).

 

Clinical classification of shock:

–         traumatic shock;

–         haemorrhagic shock;

–         dehydration shock;

–         burn shock;

–         septic shock;

–         anaphylactic shock;

–         cardiogenic shock;

–         exotoxic shock.

 

4 Shock caused by dehydration

It is a type of hypovolemic shock, which occurs during excessive body fluid loss (not blood, because hemorrhagic shock is another shock type).

Its reasons vary greatly:

–         gastrointestinal diseases (profuse vomiting, diarrhea, loss of intestinal fluid through fistula);

–         polyuria (uncontrolled diuretic treatment, diabetes mellitus and insipidus, diuretic phase of acute renal failure);

–         fluid loss through skin and wound surface (burns, high fever);

–         inadequate infusion treatment of postoperative or comatose patients;

–         hyperventilation (rapid breathing, Kussmaul breathing, inadequate artificial ventilation parameters in case of apparatus without air humidification).

However not only the complete fluid loss can be the reason of shock, but also it’s pathological distribution into the extracellular space (intestinal cavity in case of intestinal paralysis, abdominal cavity in case of ascites, pleural cavity in case of pleurisy). This way will can also act prolonged heavy tissue inflammations (peritonitis) or massive injuries (crush-syndrome).

      In cases described above electrolytes are also lost (cations of sodium, potassium, calcium, magnesium; anions of chlorine, hydrocarbonate). It causes complex osmolar, acid-base and electrolytic disorders.

Stage of dehydration shock is evaluated according to the actual fluid loss:

less than 5% of body weight – mild dehydration

5-10% of body weight – moderate dehydration

over 10% of body weight – severe dehydration

 

Water deficiency brings lowering of cardiac output, blood pressure and central venous pressure (through decrease of blood volume returning to the heart, which leads to compensatory adrenergic vasoconstriction).

Dehydration causes body weight loss, skin and mucosa dryness, decrease of subcutaneous turgor and eyeballs tone, hypothermia, tachycardia, oliguria, thirst. While dehydration progresses compensatory mechanisms weaken and central nervous system suffers: patients become sluggish, confused; hallucinations, cramps and unconsciousness are also possible. Laboratory tests show blood concentration.

One of the most important things in treatment of dehydrated patients is daily balance of fluid: check it carefully trough measuring of daily received and lost fluids (food, infusions, stool and urine output). In case of fever or tachypnea make necessary corrections. Balance should be calculated every 12-24 hours (special paper forms make this easier).

 

Daily fluid balance is calculated by adding all the received fluids (both enteral and parenteral ways) and deducting urine output, stool, perspiration and breathing water loss.

You should remember, that perspiration depends on body temperature: in case of normal temperature (36,6ºC) patient looses 0,5 ml/kg of water during every hour; 1 degree of temperature elevation adds 0,25 ml/kg to normal value of 0,5 ml/kg.

According to the fluid balance infusion therapy is divided into positive (for dehydrated patients), negative (for overhydrated patients) and “zero” (for patients without balance disorders).

Water deficiency is calculated according to the formula:

W _def = (Ht_p-Ht_n)* 0,2 BW/ Ht_n,

W _{def –} water deficiency, l;

Ht_{p –} hematocrit of the patient, l/l;

Ht_n –  normal hematocrit, l/l;

BW – body weight, kg.

Use crystalloids to treat water deficiency: saline solution, Ringer’s solution, Ringer-lactate solution, electrolytic solutions, 5%, 10, 20% glucose solution. To control potassium concentration (during dehydration this cation is widely lost) prescribe polarizing GIK mixture (pic.9.4), but don’t you ever infuse concentrated potassium solutions quickly – it can cause cardiac arrest (not more than 400 of GIK solution ml per hour).