Critical States

7/30/2019 Critical States

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Critical statesin surgery


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COMA is a condition of abrupt inhibition ofhigher nervous activity manifested by a loss ofconsciousness, disorder of all analyserfunctions: motor, skin, visual, auditory,olfactory and of inner organs.

Coma should be distinguished from soporificstate when some elements of consciousnessand reaction to strong stimuli are retained. It

should also be distinguished from stupor forwhich numbness (catalepsy) is characteristicbut with retained consciousness (these statesare provoked by psychotropic drugs but theyseldom induce coma).


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Main causes of coma:

1. Drunkenness with acute intoxication(60%).

2. Cranial trauma (25%).

3. Poisoning by barbiturates, opiate drugs.

4. Infectious meningitis and encephalitis.

5. Uremia.

6. Diabetes mellitus.

7. Hypoxia in shock and respiratory failure.

8. Epilepsy.


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COMA

Body temperature is taken. A highertemperature points to a possible infection(meningitis) or heat stroke. Hypothermia istypical of alcoholic and other types ofintoxication.

External inspection: injuries (especially ofskull), skin colouring (cyanosis points tohypoxia), edema, dilated veins in the abdomenand chest.

Cranial X-ray is compulsory. The pupils are examined (their size, reaction to

light).


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COMA Neuropathologist is called for consultation.

It is important to note the smell of the patient's breath(diabetes or acidosis are accompanied by the smell ofacetone; in hepatic coma there is a mouldy smell, inuremic coma there is a smell of urine. The smell of

alcohol is well known). If poisoning is suspected gastric contents are

examined for the presence of toxic substances.

Blood and urine sugar is investigated.

Electroencephalogram is made to assess cerebralfunctions.

Spinal puncture is done and liquor pressure is

determined (normally it should be below 300 ml).


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Conservative treatment of coma of anyetiology is aimed at prevention of

cerebral edema:

local hypothermia

diuretics: lasix, furosemid (up to 100mg)

continuous artificial lung ventilation with

oxygen content over 50%

large glucocorticosteroid doses.


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OUTCOMES OF COMA CAN BE ASFOLLOWS:

Restoration of central nervous activity;

Death of the brain.

So-called Harvard criteria of cerebral death have

been developed. To certify death all four criteriashould be present:

complete lack of verbal contact or reaction to any

stimulus; no coordinated or spasmodic movements;

complete depression of all reflexes;

complete lack of any activity in encephalogram.


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Shock is diagnosed on the basisof the following signs:

Anxiety, unclear consciousness

Dyspnoea

Tachycardia

Reduced amplitude of arterial pressure, lowarterial pressure

Cold, moist skin of pale cyanotic or marble

colouring Abrupt slowdown of blood flow in the nail bed

(that is, blocked microcirculation)

Oliguria.


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Despite this variety there aregeneral regularities of shock

development: pronounced disturbance of systemic

haemodynamics, of regionary bloodflow and microcirculation

insufficient oxygenation of various

tissues and organs leading topronounced metabolic disorders

progressing course


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The following classifications ofshock are used most often

nowadays: 1 - HYPOVOLEMIC shock due to external and internal

blood loss in burns, tissue damage, intestinal

obstruction. 2 - CARDIOGENIC shock associated with reduced

cardiac output due to the disorder of myocardialcontractile ability (myocarditis). Cardiac tamponade,

embolism of pulmonary artery. 3 - SEPTIC or infectious-toxic shock develops due to a

large amount of free toxins circulating in the blood.

4 - ANAPHYLACTIC shock is due to the development

of a severe allergic reaction.


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Treatment of shock Relief of pain: rest, warming, administration

of painkillers (narcotic drugs, neuroleptics),novocain block, immobilisation in case offracture or extensive wound, sparingtransportation.

Elimination of respiratory failure: restorationof patency of airways, administration ofmoist oxygen, if ineffective - artificial lung

ventilation is given. Restoration of cardiac and vascular function:

arrest of bleeding, replenishing the bloodloss (like in hemorrhagic shock).


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Treatment of shock To stimulate vascular tone, after circulating blood

volume is replenished, vasopressors are indicated(noradrenalin 1:1000 1-2 ml in 500 ml of 5%glucose or polyglucin solution, 1 ml of 1% mesatonsolution, 1-2 ml of 5% ephedrine solution).

Antihistamine drugs (dimedrol, pipolfen).Administration of corticosteroids in large doses (up

to 10-15 mg/kg of hydrocortisone).

To counteract acidosis soda or trisamine solutionintravenously.

Correction of electrolyte imbalance by administeringpotassium, calcium, magnesium solutions.

Counteraction of oliguria, anuria.

Gi i i f i t f i th f


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Giving infusion-transfusion therapy forhemorrhagic shock the physician has to

solve the following four tasks:

Restoration of central haemodynamics (that is,to raise the arterial pressure) by eliminating the

deficiency of circulating blood volume.Polyglucin (up to 800 ml) compensates forhypovolemia the fastest. However at this stagethe rate of replenishing blood loss is more

important than the quality of the administereddrug so it is better to start transfusing salinesolution immediately than to waste time looking

for special drugs.


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Restoration of microcirculation bynormalizing rheologic properties of

blood: reducing its viscosity,eliminating the congestion, restoringcapillary blood flow. The best drug to

do this is rheopolyglucin in the amountof 500-800 ml.


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Normalisation of transcapillary exchange (duringblood loss interstitial fluid passes over to

bloodstream the phenomenon of haemodilutionleading to intratissue dehydration. Thus, taskthree is to restore the volume of interstitial fluidby administering crystalloid solutions which getfreely through the vascular wall into interstitialspaces. These are sodium chloride, Ringerssolution etc.

Normalisation of oxygen capacity of blood.


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Acute respiratory failure (ARF)

is a condition rather than adisease; it develops acutely within

a short time period when the lungscannot provide normal partialpressure of oxygen and carbon

dioxide when compensatorymechanisms are under maximum

strain.


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Ventilation ARF

is due to insufficient ventilation ofpulmonary tissue. In this condition

blood oxygenation and removal ofcarbon dioxide is made more difficult. Itis manifested by arterial hypoxemia

(reduced partial pressure of oxygen)and hypercapnia (increased partialpressure of carbon dioxide).


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Parenchymatous ARF (hypoxemic)

develops in imbalance betweenventilation and circulation in

pulmonary capillaries; it ismanifested by arterial hypoxemia(hypercapnia in this condition

develops only at final stages ofARF).


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The immediate causes ofparenchymatous respiratory

failure can be as follows: Traumatic, hemorrhagic, cardiogenic, septic

(toxic-infectious) shock.

Acute inflammatory lung diseases (severepneumonia, pulmonary abscess etc).

Sever intoxication (peritonitis, phlegmon,

uremia etc). Lung atelectasis

Massive blood transfusion and artificialcirculation (in open heart surgery).


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There are four main signs of ARF:

Acute respiratory disorder, dyspnoea.

Reduced partial pressure of oxygen in

arterial blood below 50 mm Hg (6.7kPa) in breathing with air.

Increase in partial pressure of carbon

dioxide in arterial blood over 50 mmHg.

Decrease in pH of arterial blood below

7.3.

A t i t di d


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Acute respiratory disorder,dyspnoea.

Tachypnoe ainvolving accessory musculature passingover to apnoeasigns of progressing hypoxia andhypecapnia (tachypnoea exceeding 35 per minute is asign of decompensated respiration);

Wheezing breathing pulling in supraclavian regionsisobserved in obstruction of superior airways;

Chain-Stokes respiration, bradypnoeadevelops incerebral lesions with compression of the brain, in

poisoning with narcotic drugs and other substances; Kussmauls noisy respirationis noted in profound

metabolic acidosis in uremic, diabetic, hepatic coma);

Gasping agonal breathing characterized by

aprolonged inspiration and short expiration.


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There are main causes of lungedema:

Increased hydrostatic pressure inpulmionary vessels

reduced oncotic pressure of plasma

increased permeability of vascular wall

in children it is also the insufficiency ofsurfactant.


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Etiology ofadult respiratorydistress-syndrome

accident (aspiration of water or acid gastriccontents),

action of drugs, inhalation of poisonous gases, inhalation of concentrated oxygen (the

damaging action of oxygen usually becomesapparent 24 hours after inhalation),

disease (pneumonia, sepsis, pancreatitis,

diabetic ketoacidosis, eclampsia, shock of anyetiology),

extensive mechanic trauma, artificial circulation,

microembolism of pulmonary circulation, etc.


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Treatmentofadult respiratorydistress-syndrome

There is no specific treatment for ARDS. Thetherapy should be aimed at eliminating hypoxia byimproving all the components of oxygen transport:

pulmonary component (improvement ofventilation);

circulatory one (improvement of pumping functionof heart, decrease of peripheral vascular

resistance, restoration of circulating blood volume) hemic arrest of anemia

tissue component (improvement ofmicrocirculation)


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The cause of acute renal failure is mostoften poisoning by various substances

toxic to kidneys:

carbon butaoxide (renal affection in 96% of

cases);

death cup mushroom (95%);

acetic acid (51%)

phosphorus-organic insecticides (40%)

ethylene glycol, methyl alcohol.

CLASSIFICATION f d t d


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CLASSIFICATION of decompensated

ACUTE HEPATIC-RENAL FAILURE

1 period of early clinicalpresentations. This period correspondsto early period in poisoning or afterendotoxic, traumatic, immune conflict,hemotransfusion, septic, postoperativeor other type of shock. The clinicalpresentations are varying depending onthe etiologic factor.


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CLASSIFICATION of decompensatedACUTE HEPATIC-RENAL FAILURE

2 period of pronounced clinical presentationsor oliguria. The urine becomes dark. Its volumeis 0-500 ml/day. The body is hyperhydrated:

- pulmonary edema - - brain edema - - anasarca -

- ascitis.Laboratory signs: hyperkalemia, hypoalbuminemia,

combined decompensated acidosis, anemia,hyperchloremia, jaundice, coagulopathy,

increased urea creatinine level in blood.In fluid loss occurs due to vomiting, diarrhea,sequestration of liquid then signs of insufficientperipheral supply (lymph circulation) develop.

Development of coma is the most severeprognostic sign.


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3 period of early diuresis (restoration ofdiuresis)

Daily volume of urine gradually increases

and can be normal but the ability toconcentrate urine is not restored yet(epithelium of tubules is not regeneratedyet). So in loss of fluid the concentrationof toxins in tissues increases andencephalopathy can be aggravated.


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4 period of polyuria.

Diuresis increases within 2-3 weeks but theconcentration ability of kidneys remainslow for another 3-7 months. So thefollowing phenomena are preserved:

Hypokalemia - - hyponatremia - -

hypohydration.


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5 period of gradual clinical recovery(lasts for up to 6 mionths). Catabolism

turns into anabolism:- body weight increases - - asthenisation

persists - - low level of general protein -

- low level of intracellular electrolytes.


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TREATMENT ACUTE HEPATIC-RENAL FAILURE Surgical treatment:

opening the abscess or focus of inflammatory destruction,

sanating it; restoring blood circulation Conservative treatment:

infusion with control of diuresis, plasma proteinconcentration, ECG, circulating blood volume, potassium,

chlorine, hemoglobin. Antibacterial therapy

Detoxication:

hemodialysis

ultrafiltration hemodifiltration

hemosorption

lymphosorption

plsmapheresis

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Critical States