Method for evaluating metabolism and cerebral oxygen transport system in patients with severe cranial trauma

FIELD: medicine, resuscitation.

SUBSTANCE: one should detect cerebral perfusion pressure (CPP), intracranial pressure (ICP), values for blood saturation with oxygen in radial artery and jugular vein bulb (SaO2, SjO2), additionally one should study lactate level in jugular vein bulb and radial artery, calculate venous-arterial difference according to lactate (▵lactate), cardiac ejection (CE) due to thermodilution and hemoglobin level. Values for cerebral oxygen transport function should be calculated by the following formulas: mĎO2 = 0.15 x CE x CaO2 x 10; mVO2 = 015 x CE x (CaO2 - CjO2) x 10; CaO2 = 1.3 x Hb x SaO2; CjO2 = 1.3 x Hb x SjO2. In case of noninvasive detection - due to pulsoxymetry one should measure peripheral saturation (SpO2), due to parainfrared spectroscopy - cerebral oxygenation (rSO2) and cardiac ejection due to tetrapolar rheovasography (CEr), detect and calculate the values of cerebral oxygen transport system according to the following formulas: mĎO2 = 0.15 x CEr x CaO2 x 10; mVO2 = 0.15 x CEr x (CaO2 - CjO2) x 10; CaO2 = 1.3 x Hb x SpO2; CjO2 = 1.3 x Hb x rSO2. At the value of mĎO2 86-186 ml/min and more, MVO2 33 - 73 ml/min, ▵lactate below 0.4 mM/l one should evaluate cerebral oxygen transport system to be normal and the absence of cerebral metabolic disorders. At mĎO2 values below 86 ml/min, mVO2 being 33-73 ml/minO2, ▵lactate below 0.4 mM/l one should state upon compensated cerebral oxygen transport system and the absence of metabolic disorders. At mĎO2 being below 86 ml/min, mVO2 below 33 mM/l, ▵lactate below 0.4 mM/l one should conclude upon cerebral oxygen transport system to be subcompensated at decreased metabolism. At the values of mĎO2 being 86-186 ml/min and more, MVO2 below 33 ml/min, ▵lactate below 0.4 mM/l one should establish subcompensated cerebral oxygen transport system at decreased metabolism. At values of lactate being above 0.4 mM/l and any values of mĎO2 and mVO2 one should point out the state of decompensation in cerebral oxygen transport system and its metabolism. The innovation enables to diagnose disorders and decrease the risk for the development of secondary complications.

EFFECT: higher efficiency and accuracy of evaluation.

1 cl, 3 ex, 1 tbl

 

The method relates to medicine, namely to resuscitation.

In patients with severe traumatic brain injury develop secondary changes resulting in brain damage: they create an imbalance between consumption and oxygen and thereby cause the formation of diffuse or focal cerebral hypoxia and ischemia. Therefore, the problem of adequate monitoring of the oxygenation of the brain appears to be especially important. Cerebral blood flow (MK) is in strict accordance with the consumption of oxygen by the brain. Alone he maintained at about 50 ml/min/ 100 g brain tissue, despite substantial fluctuations in the values of mean arterial pressure (Map.). When the reduction Map. develops vasodilatation of cerebral vessels and in hypertension, on the contrary, they vasoconstriction. This process called autoregulation necessary to maintain local values of the voltage CO2permanent. Autoregulation is the main component - responsive regulatory system, working through the pCO2that requires only 30 seconds to 30 minutes to bring the vascular system to the initial state. This system is based on the effect of metabolic mediators, such as derivatives of arachidonic acid, ATP, pH, etc. So acute changes in blood pressure is still cause temporary shifts MK. Cells delivered more oxygen than they can use. At high oxygen consumption (e.g., during exercise) increased demand is compensated by the increase in cardiac output. However, low cardiac output, low hemoglobin (anemia) or low saturation of hemoglobin will lead to inadequate delivery of oxygen if there is no compensatory changes in one of the following links. On the other hand, if oxygen delivery is reduced to the level of oxygen consumption, tissue begin to extract greater amount, (saturation of the mixed venous blood falls below 60%). Reduction of oxygen delivery cannot be compensated by increasing the extraction of blood oxygen and leads to anaerobic metabolism and lactate-acylase. Known methods of assessment of oxygen delivery to the brain or consider saturation flowing and flowing oxygen (pariprasnena spectrometry; invasive determination in the carotid artery and jugular vein)or treated cerebral perfusion, intracranial, mean arterial pressure and on the assessment of these parameters is judged on the state of the brain and the effectiveness of treatment. Not calculated metrics such as delivery and consumption of oxygen by the brain, not computed venous-ar is erianna the difference in lactate (Alactic), these indicators allow us to objectively assess the state of the system of transport of oxygen to the brain and metabolism.

Known calculation method and measurement of the oxygen transport system: delivery, consumption, and utilization: Intensive care: Per. s angl. supplementary// editor-in-chief A.I. Martynov): GEOTAR MEDICINE, 1998. - ISBN 5-88816-025-3. The ICU book // Paul L. Marino// Philadelphia, Williams & Wilkins. - ISBN 0-8121-1306-3. - P.27-35.

The method is to determine the oxygen content of blood, which is found in two forms: associated with hemoglobin (Hb) and in dissolved or free state. The total amount of gas in both fractions is called the oxygen content in the blood (Sao2). The oxygen content in the arterial blood is determined taking into account the level of Hb equal to 14 grams.%, saturation of Hb with oxygen (SaO2=98%) and partial pressure of O2(pO2in the blood (PAO2), which is 100 MRTT: CaO2=(1,3×Hb×SaO2)+(0,003×paO2)

The first part of equation (1,3×Hb×SaO2) represents the oxygen content, United with Hb, and indicates that 1 gr. Hb binds at full saturation (SaO2=100%) 1.3 ml of oxygen. The second part of equation (0,003×paO2) represents the number of oxygen dissolved in the plasma component of 0.003 ml/About21 ml of plasma.

When it is required to emphasize, the contribution values RAO2in the oxygen content in the arterial blood is not significant. Thus, despite the popularity of measurement paO2this figure does not reflect the degree of blood oxygen saturation. Much more informative to assess the oxygenation of arterial blood is an indicator of SaO2a measurement RAO2it is advisable to evaluate the effectiveness of gas exchange in the lungs.

The delivery of oxygenrepresents the rate of transport of oxygen in arterial blood, which depends on the cardiac output (SW.) and oxygen content in arterial blood. OKdetermine when CaO2equal to about 18%, and cardiac index (SI)of 3 l/(min·m2) (ST, divided by the surface area of the body):

where 10 is the conversion factor volume percent in ml/s

Normal valuesrange from 520 to 720 ml/(min·m2).

Oxygen consumption (VO2) is the final stage of the transport of oxygen to the tissues and represents the oxygen supply of tissue metabolism. Equation Fika determines oxygen consumption as derived cardiac index (SI) and arteriovenous difference in the content of acid is kind (Sao 2-CvO2).

VO2=SI×(CaO2-CvO2)=SI×(13×Hb)×(SaQ2-SvO2)

Selection expressions (13×Hb) is due to the fact that it is a separate part in the above formula, which determines the oxygen content. Normal values of cardiac index 2.5-3.5 l/(min·m2) the value of VO2ranges from 110 to 160 ml/(min·m).

Most tissues are not able to store oxygen for future use (except muscle; for example, skeletal muscles retain oxygen by myoglobin can bind up to 14% of the total amount of oxygen in the body), so the absorption of oxygen from the capillaries is dependent on metabolic needs (except for violations of the ability to extract oxygen from capillary blood). When the absorption of oxygen deteriorates the indicator VO2will determine the rate of metabolic processes. This situation usually occurs in patients who are in critical conditions, and are described in detail in sepsis, multiple trauma, burns. Therefore, VO2as an indicator of the speed of metabolic processes in these cases must be determined in each patient.

The coefficient of oxygen utilization (KUO2) represents the portion of the oxygen absorbed by the tissues of the capillary is about channel; KUO2determine the ratio of oxygen consumption to its delivery:

The speed of delivery of oxygen under normal conditions significantly higher than consumption, resulting in only a small fraction of the available oxygen is extracted from the capillary blood in the normal state (at rest KUO2=22-32%). This allows the tissues to adapt to the reduction of oxygen delivery by increasing its utilization. KUO2when heavy muscular work can go up to 60-80%.

This method reflects changes occurring in the body as a whole, but does not allow to evaluate the processes occurring in the system of oxygen transport to the brain, and its metabolism in patients with severe traumatic brain injury.

The known method of non-invasive determination of cerebral oximetry in pariprasnena range as an integrated indicator of compliance delivery and consumption by the brain of oxygen and vascular regulation: Svinarenko, DSC (in Dinteren, Use, Deltaplanom, Aversin. Cerebral oximetry in pariprasnena range. The possibilities for use in neuroregeneration branch.//Anesthesiology and resuscitation. - 1998 - No. 4 - S.43-47.

The way cerebral oximetry is that a special sensor is placed on pre-processing Tannoy, free from the scalp, the skin of the patient. Preferred is the location of the sensor on one of the frontal areas. Via cable sensor is connected with the oximeter; on the screen are the current values of the saturation of cerebral blood in the studied region of the brain, but also the trend indicator. It reflects the saturation of the blood brain and not the scalp: Cerebral oximetry in dead subjects./Schwarz G.,Litscher G., Kleinert R, et al."//J Neurosurg Anest. - 1996. - 8(3). - P.189-93, and venous, since it is known that the cerebral vascular bed of the brain is 80% of the venous vessels. Discusses changes in cerebral oxygenation in the recurrence of intracranial hematomas, dependence on medication influences on the location of the sensor, changes in blood flow.

The disadvantage of this method that is diagnosed cerebral ischemia, changes over time, but does not address the relationship of changes in indicators of cerebral oxygenation (rSO2), peripheral saturation (SpO2) and indices of Central hemodynamics, not calculated parameters such as shipping (DO2), consumption (VO2) oxygen arteriovenous difference of lactate (Alactic), which allow to judge about the disturbances in the system of oxygen transport to the brain and its metabolism.

The known method, selected as a prototype, correction artery the school hypertension in the practice of intensive care patients with craniocerebral trauma and vascular brain diseases: Svinarenko, DSC (In Dinteren, Use, Deltaplanom. Correction of hypertension in the practice of intensive care patients with craniocerebral trauma and vascular diseases of the brain.//Bulletin of intensive therapy. - 1999 - No. 2.

The essence of the method is that the estimation of cerebral blood flow, using the indicator of cerebral perfusion pressure (JRC) is the difference between the mean arterial pressure and intracranial pressure. Mean arterial pressure (SAD) is calculated by the formula: GARDEN=Addict.+Hell pulse/3, where the Hell pulse=Adsit.-Addict. Thus, the GARDEN is located between the systolic and diastolic pressures, closer to diastolic. This indicator is widely used in neurosurgery to calculate the perfusion pressure of the brain: JRS=GARDEN-ICP. Normal JRS equal to 80 mm Hg; when reduced to 50 mm Hg arise metabolic signs of ischemia and reduced electrical activity of the brain. Several studies on patients with severe traumatic brain injury has been shown to increase mortality and poor outcomes in the fall JRS<70 mm Hg for a long time. Constant monitoring of the blood saturation in the jugular vein is another important method of monitoring the adequacy of cerebral blood flow. Saturation in the jugular vein (SjO2 ) reflects the saturation of venous blood that drains from the cavity of the skull, which in norm equal to 65-75%. If the blood flow is reduced to a critical level, begins to decrease venous saturation (rSO2), that is, to maintain the flow of oxygen to the brain begins to consume more oxygen from the blood.

To maintain the optimum HELL and JRS is highly informative comparison of these figures with the data arteriovenous difference in oxygen (AVDO2 - arterio - venous difference). The increase in AVDO2 may reflect both the potential risk of ischemic changes due to decreased blood flow, and to be a real manifestation of ischemic neurons with increased oxygen consumption. Calculation AVDO2 can be done by invasive determination of hemoglobin saturation with oxygen in the blood of the carotid artery and jugular vein, and using non-invasive indicators. For non-invasive assessment of hemoglobin saturation with oxygen in the arterial blood pulse oximetry is used in venous blood brain pariprasnena spectroscopy (cerebral oximetry - rSO2). The possibility of this approach is explained as follows. With sufficient accuracy can be considered as the saturation of hemoglobin in different arteries of the same. Therefore, non-invasive assessment of this indicator using pulse oximetry (SpO2) close to the value at which ysenia hemoglobin in the arteries (SaO 2)supplying the brain, at the same time cerebral oxygenation (rSO2) reflects the saturation of hemoglobin with oxygen in the brain tissue.

The disadvantage of this method is that used in the way diagnostic methods do not allow to assess deficiencies in the system of oxygen transport to the brain, as well as the status of the compensation mechanisms of the metabolism of the brain.

The purpose of this method is the early assessment irregularities in the transport of oxygen to the brain, and the mechanisms required for normal metabolism of the brain with the aim of preventing and reducing the risk of developing secondary complications.

This object is achieved in that the admission of the patient to the intensive care unit determined in the absence of contra-indications: cerebral perfusion pressure (JRC), intracranial pressure (ICP), measure the performance of the oxygen saturation of blood in the radial artery and the jugular bulb Vienna (SaO2, SjO2additionally examine the level of lactate in the bulb jugular vein and radial artery determine venous-arterial difference for lactate (Δlactate) for assessment of cerebral metabolism, cardiac output (SV) method thermodilution, hemoglobin level, calculate the indicators of the transport function of oxygen to the brain n the formulas:

VO2=0,15×ST×(CaO2-CjO2)×10;

Sao2=1,3×Hb×SaO2;

CjO2=1,3×Hb×SjO2,

where

CaO2- the amount of oxygen in arterial blood (%);

1,3 - amount of oxygen associated 1G. hemoglobin at full saturation (ml);

Hb - the amount of hemoglobin (g%);

SaO2- saturation of arterial blood with oxygen;

CjO2- the amount of oxygen the blood in the jugular vein (%);

SjO2the oxygen saturation in the jugular vein;

- delivery of oxygen to the brain;

0,15 - factor, allowing to investigate the performance of the transport of oxygen to the brain;

SV - cardiac output;

10 is the conversion factor volume percent in ml/s;

VO2the oxygen consumption of the brain;

- 86-186 ml/min;

VO2- 33-73 ml/min

When values of86-186 ml/min or more, VO233-73 ml/min, Δlactate less than 0.4 mmol/l assess the system of oxygen transport to the brain of normal and absence of metabolic disorders of the brain.

Whenless than 86 ml/min, VO233-73 ml/min, Δlactate less than 0.4 mmol/l assess the condition of the transport of oxygen to the brain compensated and absence of metabolic disorders of the brain.

When86-186 ml/min or more, VO2more than 73 ml/min, Δlactate less than 0.4 mmol/l assess the condition of the transport of oxygen to the brain compensated and increase metabolism.

Whenless than 86 ml/min, VO2less than 33 mmol/l, Δlactate less than 0.4 mmol/l assess the condition of the transport of oxygen to the brain subcompensated and decrease metabolism.

When86-186 ml/min or more, VO2less than 33 ml/min, Δlactate less than 0.4 mmol/l assess the condition of the transport of oxygen to the brain subcompensated and decrease metabolism.

When the values Δlactate more than 0.4 mmol/l and any values ofand VO2assess how the state of decompensation in the system of oxygen transport to the brain and its metabolism.

To reduce the risk of complications of invasive investigation of SaO2you can replace the peripheral dimension of the blood saturation (SpO2using the method of pulse oximetry, a SjO2- cerebral oxygenation (rSO2), as measured by the method pariprasnena spectrometry, using in the calculation. Invasive determination of the SV method thermodilution replace the non-invasive measurement method tetrapolar rheovasography (SVR). The ability of this approach obyasnyau the SJ as follows. With sufficient accuracy can be considered as the saturation of hemoglobin in different arteries of the same. Therefore, non-invasive assessment of this indicator using pulse oximetry close to the magnitude of the saturation of hemoglobin in the arteries supplying the brain, at the same time cerebral oxygenation reflects the saturation of hemoglobin with oxygen in the brain tissue. They expect the performance of the transport function of oxygen to the brain by the formulas:

VO2=0,15×SWR×(CaO2-CjO2)×10;

CaO2=1,3×Hb×SpO2;

CjO2=1,3×Hb×rSO2,

where

- delivery of oxygen to the brain;

VO2the oxygen consumption of the brain;

SVR - cardiac output obtained by the method of tetrapolar rheovasography;

0,15 - coefficient taking into account the transport of blood to the brain;

10 is the conversion factor volume percent in ml/s;

Sao2- the amount of oxygen in arterial blood (%);

1,3 - amount of oxygen bound 1 gr. hemoglobin at full saturation (ml);

Hb - the amount of hemoglobin (g%);

SpO2- saturation of capillary blood by oxygen;

CjO2- the amount of oxygen the blood in the jugular vein (vol.%);

rSO2- oxygen saturation Ott is flowing from the brain to the blood;

To conduct corrective therapy to control transport of oxygen to the brain in an unstable state after 8 hours, and after stabilization of the patient - at least once a day. Monitoring of oxygen transport stop by stabilizing the patient's condition and the formation of a persistent vegetative state, or the regression of cerebral symptoms (score coma scale Glasgow above 9-10 points).

The novelty of the method:

- additionally calculate the indicators of the transport of oxygen to the brainVO2on the proposed formulas;

- in addition to measuring the level of lactate in the jugular vein and radial artery, expect venous-arterial difference for lactate (Δlactate);

- used for calculations cardiac output (SV.), multiplied by a correction factor of 0.15, as only 15% of the ST provides the cerebral blood flow, and oxygen saturation of blood in the jugular vein (SjO2);

for86-186 ml/min and more VO233-73 ml/min, Δlactate less than 0.4 mmol/l, estimate the system of oxygen transport to the brain of normal and absence of metabolic disorders of the brain;

- whenless than 86 ml/min, VO233-73 ml/min, Δlactate less than 0.4 m the ol/l assess the condition of the transport of oxygen to the brain compensated and absence of metabolic disorders of the brain;

- when86-186 ml/min or more, VO2- 73 ml/min, Δlactate less than 0.4 mmol/l assess the condition of the transport of oxygen to the brain compensated and increase metabolism;

- whenless than 86 ml/min, VO2less than 33 mmol/l, Δlactate less than 0.4 mmol/l assess the condition of the transport of oxygen to the brain subcompensated and decrease metabolism;

- when86-186 ml/min or more, VO2less than 33 ml/min, Δlactate less than 0.4 mmol/l assess the condition of the transport of oxygen to the brain subcompensated and decrease metabolism;

for Δlactate more than 0.4 mmol/l and any values ofand MVO2assess how the state of decompensation in the system of oxygen transport to the brain and its metabolism;

- to reduce the risk of complications is proposed to replace invasive measurement of SaO2on SpO2(pulse oximetry), SjO2on rSO2(pariprasnena spectrometry, a measure of cerebral oxygenation), and measurement of SV method thermodilution on SVR (method tetrapolar rheovasography), calculated by proposed formulas;

- monitoring of oxygen transport spend every day: when an unstable state after 8 hours, last the stabilization performance delivery and consumption, and Δlactate for at least 1 times a day, after stabilization of the patient, forming a persistent vegetative state or regression of the rate of loss of consciousness up to 9-10 points on a scale Glasgow coma that control ceased.

The proposed method allows to reveal early disturbances in the system of oxygen transport and state mechanisms for the metabolism of the brain (see above), that allows to correct treatment and reduce the risk of complications. This provides pathogenetically grounded approach in the treatment, consistency and validity of actions when exposed to broken links in the system of oxygen transport to the brain and its metabolism.

The essence of the method lies in the fact that the admission of a patient with severe traumatic brain injury in the intensive care unit in the absence of contraindications measured intracranial pressure (kateteriziruyut the ventricles of the brain, epidural, or endolyumbalno space), cerebral perfusion pressure (calculated according to the formula JRS=AD cf - ICP). Examines indicators of blood oxygen saturation in the jugular bulb vein and radial artery (SjO2, SaO2). Additionally measure the cardiac output method thermodilution (SW), the level of hemoglobin and lactate is Rove in the jugular vein, calculate the indicators of oxygen transport to the brain:

VO2=0,15×ST×(CaO2-CjO2)×10,

where

- delivery of oxygen to the brain;

VO2the oxygen consumption of the brain;

SV - cardiac output;

0,15 - factor, allowing to investigate the performance of the transport of oxygen to the brain, because it provides only 15% of cardiac output: B. Volkov, E. Neil. The circulation. // Moscow. Medicine. - 1976 - s.(total 463), i.e. in this case the organ blood flow;

10 is the conversion factor volume percent in ml/s;

CaO2- the amount of oxygen in arterial blood (vol.%), determined by the formula:

CaO2=1,3×Hb×SaO2,

where

SaO2- saturation of arterial blood with oxygen;

1,3 - oxygen link 1 gr. hemoglobin at full saturation (ml);

Hb - the amount of hemoglobin (g%);

CjO2- the amount of oxygen the blood in the jugular vein (%) determined by the formula:

CjO2=1,3×Hb×SjO2,

where

SjO2the oxygen saturation in the jugular vein;

For the evaluation of cerebral metabolism determine the level of lactate in the radial artery and jugular vein, calculate venous-arterial times the Itza (Δ lactate). When the values Δlactate 0.4 mmol/l talk about decompensation system transport oxygen to the brain and the processes of its metabolism. For normal values of lactate in the artery and vein to calculate the critical level of the venous-arterial difference data taken from reference: encyclopedia of clinical laboratory tests.// Under the editorship of Professor Norbert U. of TIC. // Translation from English. CH. editor Professor Menshikov V.V. // Publishing house "Laboratory", Moscow, 1997, str-290.

When registering deviations from normal values begin corrective therapy to improve the transport of oxygen to the brain and prevention of disorders of metabolism.

Corrective therapy includes:

1) elimination of volemic violations - increase infusion, when the pressure exceeds jamming pulmonary capillaries (ZLC) 18 mm Hg shows the use of drugs and inotropic cardiotonic action, such as dopamine at a dose of 4-7 µg/kg/min;

2) using the modes and methods of respiratory support with minimal impact on pulmonary and Central hemodynamics (ventilation, controlled pressure) to reduce the negative impact on SV;

3) normalization of gas exchange - correction of anemia, ventilation and diffusion function the lung;

4) reduction in ICP at rise above 15 mm Hg;

5) the use of thiopental sodium at a dose of 4-5 mg/kg to reduce the activity of the brain or other drugs;

6) the use of dalargin - 2 mg 6 times a day, as it has anti-ischemic and cytoprotective effect;

7) the use of moderate hypothermia 33-35°in the esophagus.

When values of86-186 ml/min or more, VO233-73 ml/min, Δlactate less than 0.4 mmol/l is judged on normal delivery and oxygen consumption by the brain, about the absence of metabolic disorders of the brain.

Whenless than 86 ml/min, VO233-73 ml/min, Δlactate less than 0.4 mmol/l is judged on the reduction of oxygen delivery to the brain and compensate by increasing the extraction, for normal usage, the lack of metabolic disorders of the brain.

To prevent further worsening of conduct violations corrective therapy for items 1, 2, 3, 4.

When86-186 ml/min or more, VO2more than 73 ml/min, Δlactate less than 0.4 mmol/l assess the condition of the transport of oxygen to the brain compensated and increase metabolism.

To prevent further worsening of conduct violations corrective therapy aimed at reducing metabolic need to change the capacity of the brain to paragraphs 5, 6, 7, 4.

Whenless than 86 ml/min, VO2less than 33 mmol/l, Δlactate less than 0.4 mmol/l assess the condition of the transport of oxygen to the brain subcompensated and decrease metabolism, in this case, correctionand VO2on points 1, 3, 2, 4.

When86-186 ml/min or more, VO2less than 33 ml/min, Δlactate less than 0.4 mmol/l assess the condition of the transport of oxygen to the brain subcompensated and decrease metabolism. Is the sequence of actions in sleduushem order 3, 2, 4, 6, 1. Is the sequence of actions in sleduushem order 3, 2, 4, 6, 1.

When the values Δlactate more than 0.4 mmol/l and any values ofand VO2evaluate how the state of decompensation in the system of oxygen transport to the brain and its metabolism, as in this situation, the flow does not meet the needs of the brain of oxygen, in this situation, conduct therapy, which includes all of the above components. The sequence of the procedures depends on the prevalence of disorders.

To reduce the risk of complications of invasive investigation of SaO2you can replace the measurement of peripheral saturation of the blood - SpO2(pulse oximetry), and SjO -rSO2, cerebral oxygenation (method-pariprasnena spectrometry), using in the calculation. Invasive determination of the SV method thermodilution replace the non-invasive measurement method tetrapolar rheovasography (SVR).

To conduct corrective therapy to control transport of oxygen to the brain, in an unstable state after 8 hours, and after stabilization of the patient - at least once a day. Monitoring of oxygen transport stop by stabilizing the patient's condition and the formation of a persistent vegetative state, or the regression of cerebral symptoms (score coma scale Glasgow above 9-10 points). Options violations presented in the table.

Table.

Status options metabolism and oxygen transport to the brain in patients with severe traumatic brain injury.
Oxygen delivery to the brain DO2(ml/min)86-186 and more.Less than 86.86-186 and more.Less than 86.86-186 and more.Any value.
The oxygen consumption of the brain VO2(ml/min)33-73.33-73. More than 73less than 33Less than 33Any value.
The state of the system of transport of oxygen to the brain.Rate.Compensation.Subcompensated.Decompensation.
The state of metabolism.No violations.Increase.Reduction.
Venous-arterial difference for lactate (Δlactate) mmol/lLess than 0.4.More than 0.4.

Clinical example No. 1.

Ill AV, case history No. 1437, was admitted to the hospital at 11 : 00 a.m. 21. 09. 01 year of Tashtagol city hospital. The state of extreme severity, the degree of loss of consciousness, coma 1 (score on a scale of whom Glasgow 7 points), diagnosis: Severe open craniocerebral injury. Brain contusion severe with compression of acute epidural hematoma of the right fronto-parieto-temporal lobe. Swelling, dislocation brain, phase of clinical decompensation. Fracture of the lower jaw on the right. Alcohol intoxication.

The diagnosis is put on the basis of survey data, which included echoencephalography, clinical and neurological examination, x-ray is logical (computer tomography, radiography of the chest), the General analysis of blood, urine.

The patient was admitted to the Department 21.09.2001, in critical condition after surgery: resection trepanation of the skull in the left fronto-parieto-temporal region, the destruction of acute epidural hematoma. During treatment (14 days) the degree of loss of consciousness regressed to moderate stun (on a scale Glasgow coma 13 points).

At admission the patient's condition is extremely serious, is artificial lung ventilation (ALV) in the mode control pressure, hemodynamics offset: blood pressure (BP) is 140/90 mm Hg, pulse (Ps) - 100 in 1 min, Central venous pressure (CVP) - 5 mm Hg, sampled from the radial artery and the bulb of the jugular vein to determine the blood oxygen saturation and the amount of lactate, capillary blood to determine the level of hemoglobin (Hb). Catheterized pulmonary artery to monitor indices of Central hemodynamics, calculation of cerebral perfusion pressure (JRC), given that the operation was drained of the anterior horn of the left lateral ventricle of the brain, produced by the measurement of intracranial pressure (ICP).

The following data were obtained: the oxygen saturation of blood in the bulb jugular vein to the right (SjO2) is 0.4, the radial artery (SaO2) - 0,98, ISM is Ren cardiac ejection method thermodilution (ST) - 2 l/min, hemoglobin (Hb) of 8.2 g.%, ICP - 10 mm Hg (normal range up to 15 mm Hg), JRC - 96,7 mm Hg (normal range not lower than 70 mm Hg). The calculated values of oxygen transportVO2by the formulas:

VO2=0,15×ST×(CaO2-CjO2)×10,

where

- delivery of oxygen to the brain;

VO2the oxygen consumption of the brain;

SV - cardiac output;

0,15 - coefficient taking into account the transport of blood to the brain;

10 is the conversion factor volume percent in ml/s;

Sao2- the amount of oxygen in arterial blood (% vol.) determined by the formula

CaO2=1,3×Hb×SaO2,

where

1,3 - oxygen link 1 gr. hemoglobin at full saturation (ml);

Hb - the amount of hemoglobin (g%);

SaO2- saturation of arterial blood with oxygen;

CjO2- the amount of oxygen the blood in the jugular vein (vol.%) determined by the formula

CjO2=1,3×Hb×SjO2;

SjO2the oxygen saturation in the jugular vein;

CaO2=1,3×8,2×0,98=10,5 (vol.%);

CjO2=1,3×8,2×0,4=4,3 (vol.%);

VO2=0,15×2×(10,5-4,3)×10=18.5 ml/min;

Δlactate - 0,39.

On the basis of the data obtained made clucene on reduction of metabolism, subcompensation reducing consumption and oxygen delivery to the brain.

Initiated corrective therapy: correction of anemia, increased volume of infusion therapy under the control of the jamming pressure pulmonary capillaries (ZLC), with an increase to 18 mm Hg below shows the connection of inotropic support, because of the high risk of development of pulmonary edema, optimized ventilation, increased percentage of oxygen in the inhaled mixture (from 25% to 40%). When the control calculation VO2and8 hours later:

SV - 5 l/min, Hb - 10 gr%, SaO2- 1, SjO2to 0.6, Δlactate - 0.3 mmol/l,

A/D - 140/90 mm Hg, ICP - 12 mm Hg, JRC - 94,7 mm Hg, Ps - 80 minutes,

CaO2=1,3×10×1=13,0 vol.%;

CjO2=1,3×10×0,6=7,8 vol.%;

VO2=0,15×5×(13-7,8)×10=39 ml/min

On the basis of the obtained data it can be concluded normal delivery and oxygen consumption by the brain, about the absence of metabolic disorders of the brain. Continued treatment and supervision.

24.09.2001, the Degree of loss of consciousness regressed to spoor (on a scale Glasgow coma 9 points). It is noted in a patient lifting a/D up to 170/110 mm Hg, Ps - 110 minutes, CVP - 40 mm Vogt, JLK - 20 mm Hg, SaO2is 0.99, SjO2is 0.55 SV - 8 l/min, Hb - 11 gr.%, Δlactate - 0.35 mmol/l, ICP 10 mm Hg, JRC - 120 mm Hg calculated indicators of oxygen delivery to the brain:

CaO2=1,3×11×0,99=14,2%;

CjO2=1,3×11×0,55=7,9 vol.%;

VO2=0,15×8×(14,2-7,9)×10=75,5 ml/min

These figures show that increasing the metabolism and compensate for the increased oxygen consumption during normal delivery.

Given the high JLC, the patient is assigned dopamine at a dose of 2 mcg/kg/min, with the goal of increasing diuresis, gradual decrease in hydration, given the high rate of consumption by the brain of oxygen appointed thiopental sodium at a dose of 2 mg/kg/min, dalargin 1 mg 3 times/day.

On therapy after 8 hours produced the control parameters of oxygen transport:

A/D - 150/90 mm Hg, Ps - 90 min, CVP - 30 mm Vogt, JLK - 18 mm Hg, SaO2is 0.99, SjO2- 0,65 SV - 5 l/min, Hb - 11 gr.%, Δlactate - 0.25 mmol/l, ICP 10 mm Hg, JRC - 100 mm Hg calculated indicators of oxygen delivery to the brain:

CaO2=1,3×11×0,99=14,2%;

CjO2=1,3×11×0,65=9,3%;

VO2=0,15×5×(14,2-9,3)×10=to 36.5 ml/min

Given the normalization of the indicators, cancelled dopamine, reduced infusion therapy due to the high values JLC.

Further there were minor fluctuations and VO2values Δlactate did not exceed 0.3 mmol/l To 14 days the patient was transferred to an independent breath, cancelled thiopental sodium, dalargin.

The degree of loss of consciousness regressed to moderate stun (on a scale Glasgow coma 13 points). Given the stable indices of Central hemodynamics, oxygen transport system to the brain with 6 days of monitoring was performed 1 time per day., and on the 8th terminated.

Clinical example No. 2.

Patient P.A., case history No. 1422, was admitted to the hospital in 19 hours 00 minutes 22.09.01. years after a criminal injury. The status of the victim of extreme severity, the degree of loss of consciousness, coma 1 (score on a scale of whom Glasgow - 7 points). After the examination, including clinical and neurological examination, x-ray computer tomography, radiography of the chest), the General analysis of blood, urine, diagnosed with Open-severe traumatic brain injury, brain contusion with compression of acute subdural hematoma in the left fronto-parieto-temporal region, with the crushing of the brain's left temporal lobe (bruised 111, a linear fracture of the occipital bone on the right), the coarse phase clinical decompensation. Contused wounds of the soft tissues of the head.

The patient was admitted to the Department 22.09.2001, in a very severe condition is AI, after surgery: resection trepanation of the skull in the left fronto-parieto-temporal region, the destruction of acute subdural hematoma were treated to 15.10.2001, During this time the patient has formed a persistent vegetative state.

At admission the patient's condition is extremely serious, initiated an artificial lung ventilation (ALV) in the mode control pressure, hemodynamics offset: blood pressure (BP) - 110/80 mm Hg, pulse (Ps) - 110 in 1 min, Central venous pressure (CVP) - 0 mm Hg produced non-invasive determination of SaO2-SpO2(pulse oximetry) and SjO2-rSO2(cerebral oximetry), measurement and calculation of SVR (tetrapolar rheovasography instead SV, measured by the method of thermodilution), the amount of lactate in the radial artery and the left jugular vein, the study of capillary blood to determine the level of hemoglobin (Hb). Calculation of cerebral perfusion pressure (JRC), given that the operation was drained of the anterior horn of the right lateral ventricle of the brain, produced by the measurement of intracranial pressure (ICP).

The following data were obtained: Cerebral oximetry right rSO2- 0,23, pulse oximetry SpO2- 0,98 measured cardiac ejection method tetrapolar rheovasography SVR - 7 l/min, hemoglobin (Hb) - 12 oz.%,ICP - 15 mm Hg (normal range up to 15 mm Hg), JRS 75 mm Hg (normal range not lower than 70 mm Hg). The calculated values of oxygen transportVO2according to the formula

CaO2=1,3×Hb×SpO2;

CjO2=1,3×Hb×rSO2;

VO2=0,15×SWR×(CaO2-CjO2)×10,

where

- delivery of oxygen to the brain;

VO2the oxygen consumption of the brain;

SVR - cardiac output obtained by the method of tetrapolar rheovasography;

0,15 - coefficient taking into account the transport of blood to the brain;

10 is the conversion factor volume percent in ml/s;

CaO2- the amount of oxygen in arterial blood (% vol.) determined by the formula:

CaO2=1,3×Hb×SpO2,

where

1,3 - oxygen link 1 gr. hemoglobin at full saturation (ml);

Hb - the amount of hemoglobin (g%);

SpO2- saturation of capillary blood by oxygen;

CjO2- the amount of oxygen the blood in the jugular vein (vol.%), determined by the formula

CjO2=1,3×Hb×rSO2;

rSO2- saturation of oxygen flowing from the brain of blood;

CaO2=1,3×12×0,98=15,3 (vol.%)

CjO2=1,3×12×0,23=3,6 (vol.%);

VO2=0,15 7×(15,3-3,6)×10=122,9 ml/min;

Δlactate - 0,49.

On the basis of the obtained data it can be concluded decompensation in the system of oxygen transport due to high oxygen consumption by the brain high metabolic activity.

Initiated corrective therapy: volume infusion therapy under the supervision of indices of Central hemodynamics, is shown holding a dehydration treatment to reduce SVR because of the high risk of development of pulmonary edema, optimized ventilation, increased percentage of oxygen in the inhaled mixture up to 30%. Assigned antihypoxant therapy, to reduce brain needs oxygen (barbituric protection - thiopental sodium at a dose of 4 mg/kg/hour, dalargin 1 mg 3 times/day.

When the control calculation VO2and8 hours later:

SV - 5 l/min, Hb - 12 gr.%, SpO2- 1, rSO2to 0.6, Δlactate to 0.39 mmol/l, a/D - 130/90 mm Hg, ICP - 14 mm Hg, JRC - 89,3 mm Hg, Ps - 100 in 1 min

CaO2=1,3×12×1=15,6%;

CjO2=1,3×12×0,6=9,36 vol.%;

VO2=0,15×5×(15,6-9,36)×10=46,8 ml/min;

Δlactate to 0.39 mmol/L.

On the basis of the obtained data it can be concluded normal delivery and oxygen consumption by the brain, about the absence of metabolic disorders leading what about the brain. Continued treatment and supervision.

24.09.2001, the Degree of loss of consciousness superficial coma (coma scale Glasgow 7 points). The underlying disease course was complicated by gastrointestinal bleeding, which stopped conservatively. The condition of the patient is stable a/D - 110/70 mm Hg, Ps - 100 in 1 min, CVP - 5 mm Vogt, SpO2- 0,98, rSO2- 0,5 SV - 4 l/min, Hb - 8,0 gr.%, Δlactate - 0.35 mmol/l, ICP 10 mm Hg, JRC - 73,3 mm Hg calculated indicators of oxygen delivery to the brain:

CaO2=1,3×8,0×0,98=10,2 vol.%;

CjO2=1,3×8,0×0,5=5,2 vol.%;

VO2=0,15×4×(10,2-5,2)×10=30,0 ml/min

These figures indicate a decline in metabolism, subcompensation reducing consumption and oxygen delivery to the brain.

The patient is assigned dopamine at a dose of 4 mcg/kg/min, increased hydration to improve the SVR, the correction of anemia, optimizirovan respiratory therapy.

On the background of treatment after 8 hours produced the control parameters of oxygen transport:

A/D - 130/90 mm Hg, Ps - 90 in 1 minutes, CVP - 20 mm Vogt, SpO2is 0.99, rSO2to 0.6 SV - 5 l/min, Hb - 10 gr%, Δlactate - 0.35 mmol/l, ICP 10 mm Hg, JRC - 93,3 mm Hg calculated indicators of oxygen delivery to the brain:

CaO2=1,3×10×0,99=12,9%;

CjO2=1,3×10×0,6=7,8 vol.%;

VO2=0,15×5×(12,9-7,8)×10=38,0 ml/min

Given the normalization of the indicators, cancelled dopamine, therapy predalien.

Further there were minor fluctuations in mand VO2values Δlactate did not exceed 0.35 mmol/l To 14 days the patient was transferred to an independent breath. Formed a persistent vegetative state. Given the stable indices of Central hemodynamics, oxygen transport system to the brain with 8 days control was performed 1 time per day., and on the 14th terminated.

Clinical example No. 3.

Patient UV, case history No. 1768, was admitted to the hospital in 19 hours 00 minutes 2. 11. 01 year, delivered by ambulance. The state of extreme severity, the degree of loss of consciousness, coma 2 (score on a scale of whom Glasgow - 5 points), diagnosis: Severe closed traumatic brain injury. Brain contusion severe with compression of acute intracerebral hematoma in the right frontal lobe. Swelling, dislocation of the head-brain, phase of clinical decompensation. Alcohol intoxication.

The diagnosis is put on the basis of survey data, which included echoencephalography, clinical and neurological examination, x-ray computer tomography, radiography of the chest), complete blood count, m is Chi.

The patient was admitted to the Department 2.11.2001, in critical condition after surgery: resection trepanation of the skull in the left fronto-parieto-temporal region, the destruction of acute intracerebral hematomas. During treatment (20 days) the degree of loss of consciousness regressed to spoor (on a scale Glasgow coma 9 points).

At admission the patient's condition is extremely serious, is artificial lung ventilation (ALV) in the mode control pressure, hemodynamics offset: blood pressure (BP) is 150/90 mm Hg, pulse (Ps) - 60 in 1 minute, Central venous pressure (CVP) - 0 mm Hg, sampled from the radial artery and the bulb of the jugular vein on the left to determine the blood oxygen saturation and the amount of lactate, capillary blood to determine the level of hemoglobin (Hb). Catheterized pulmonary artery to monitor indices of Central hemodynamics, calculation of cerebral perfusion pressure (JRC), given that the operation was drained of the anterior horn of the right lateral ventricle of the brain, produced by the measurement of intracranial pressure (ICP).

The following data were obtained: the oxygen saturation of blood in the bulb jugular vein to the right (SjO2) to 0.63 in the radial artery (SaO2) - 0,98 measured cardiac ejection method thermodilution (SW) - 4.2 l/min, hemoglobin (Hb) - 1 gr.%, ICP - 16 mm Hg (normal range up to 15 mm Hg), JRC - 94,0 mm Hg (normal range not lower than 70 mm Hg). The calculated values of oxygen transportVO2by the formulas:

CaO2=1,3×11×0,98=14,0 (vol.%);

CjO2=1,3×11×0,63=9,0 (vol.%);

VO2=0,15×4,2×(14,0-9,0)×10=31.5 ml/min;

Δlactate - 0,39.

Based on these data concluded that the decrease in metabolism, subcompensation reducing consumption and oxygen delivery to the brain.

Initiated corrective therapy: increased volume of infusion therapy under the control of the jamming pressure pulmonary capillaries (ZLC), with an increase to 18 mm Hg below shows the connection of inotropic support, because of the high risk of development of pulmonary edema, optimized artificial ventilation of the lungs.

When the control calculation VO2and8 hours later:

SV - 5 l/min, Hb - 10 gr%, SaO2is 0.99, SjO2- 0,4, Δlactate - 0.3 mmol/l, a/D - 140/90 mm Hg, ICP - 12 mm Hg, JRC - 94,7 mm Hg, Ps - 80 in 1 minute

CaO2=1,3×10×0,99=12,9%;

CjO2=1,3×10×0,4=5,2 vol.%;

VO2=0,15×5×(12,9-5,2)×10=57,5 ml/min;

Δlactate - 0,45.

Based on these data it is concluded that the patient despite the normal levels of the delivery and consumption of decompensation in the system of oxygen transport, that is not provided with metabolic needs oxygen to the brain, given the high JLC - 19 mm Hg, appointed inotropic support (dopamine 4 mcg/kg/min), to reduce brain needs oxygen - sodium thiopental 4 mg/kg/min, dalargin 1 mg 3 times/day., rheological therapy.

Continued treatment and follow-up, after 8 hours spent monitoring conducted therapy:

A/D - 150/100 mm Hg, Ps - 90 in 1 min, CVP - 40 mm Vogt, JLK - 16 mm Hg, SaO2is 0.99, SjO2- 0,65 SV - 5 l/min, Hb - 11 gr.%, Δlactate - 0.35 mmol/l, ICP 10 mm Hg, JRC - 106,7 mm Hg calculated indicators of oxygen delivery to the brain:

CaO2=1,3×11×0,99=14,2%;

CjO2=1,3×11×0,65=9,3%;

VO2=0,15×5×(14,2-9,3)×10=to 36.5 ml/min

Given the normalization of the indicators, cancelled dopamine, reduced infusion therapy due to the high values JLC.

Further there were minor fluctuationsand VO2values Δlactate did not exceed 0.3 mmol/l To 14 days the patient was transferred to an independent breath, cancelled thiopental sodium, dalargin. The degree of loss of consciousness regressed to spoor (on a scale Glasgow coma 9 points). Given the stable indices of Central hemodynamics, oxygen transport system to the brain with stock control was performed 1 time per day., and on the 8th terminated.

The proposed method is used in the intensive care unit №1 of the city clinical hospital №29, the branch of Institute PR RAMS treated 32 patients with severe traumatic brain injury, it is possible to diagnose deficiencies in the system of oxygen transport and metabolism of the brain in the early stages, to provide differential pathogenetically grounded approach in the treatment, to reduce the number of complications.

1. The method of evaluation of the metabolism and transport of oxygen to the brain in patients with severe traumatic brain injury, including the monitoring of intracranial pressure (ICP), cerebral perfusion pressure (JRC), determination of blood oxygen saturation, wherein define invasive methods saturation of arterial blood with oxygen (SaO2) and the oxygen saturation in the jugular bulb Vienna (SjO2), hemoglobin level (Hb), lactate in the bulb jugular vein and radial artery determine venous-arterial difference for lactate (Δlactate), cardiac output (SV) and calculate the indicators of the transport function of blood oxygen to the brain by the formula

VO2=0,15·ST·(CaO2-CjO2)·10;

where- delivery of oxygen to the brain is the mind, ml/min;

VO2- oxygen consumption by the brain, ml/min;

SV - cardiac output, l/min;

0,15 - coefficient taking into account the transport of blood to the brain;

10 is the conversion factor volume percent, ml/s;

CaO2- the amount of oxygen in arterial blood.% determined by the formula

CaO2=1,3·Hb·SaO2

where 1,3 - amount of oxygen bound 1 gr. hemoglobin at full saturation (ml);

Hb - the amount of hemoglobin in grams.%;

SaO2- saturation of arterial blood with oxygen;

CjO2- the amount of oxygen the blood in the jugular vein in% vol. determined by the formula

CjO2=1,3·Hb·SjO2;

SjO2the oxygen saturation in the jugular vein;

or determined by non-invasive method of peripheral pulse oximetry saturation (SpO2), method pariprasnena spectroscopy cerebral oxygenation (rSO2) and cardiac ejection method tetrapolar rheovasography (SVR), determine and calculate the indicators system of oxygen transport to the brain by the formula

VO2=0,15·SWR·(CaO2-CjO2)·10;

where SVR - cardiac output is determined by the method tetrapolar reeva is ographie, l/min;

CaO2=1,3·Hb·SpO2;

SpO2- saturation of hemoglobin in arterial blood oxygen;

the amount of oxygen in venous blood flowing from the brain, are calculated according to the formula

CjO2=1,3·Hb·rSO2;

where rSO2- saturation of venous blood flowing from the brain,

when values of86-186 ml/min or more, VO233-73 ml/min, Δlactate less than 0.4 mmol/l assess the system of oxygen transport to the brain of normal and absence of metabolic disorders of the brain;

whenless than 86 ml/min, VO233-73 ml/min, Δlactate less than 0.4 mmol/l, assess the condition of the transport of oxygen to the brain compensated and absence of metabolic disorders;

when86-186 ml/min or more, VO2- 73 ml/min, Δlactate less than 0.4 mmol/l, assess the condition of the transport of oxygen to the brain compensated and increase metabolism;

whenless than 86 ml/min, VO2less than 33 mmol/l, Δlactate less than 0.4 mmol/l, assess the condition of the transport of oxygen to the brain subcompensated and decrease metabolism;

when86-186 ml/is in and more VO2less than 33 ml/min, Δlactate less than 0.4 mmol/l, assess the condition of the transport of oxygen to the brain subcompensated and decrease metabolism;

when the values Δlactate more than 0.4 mmol/l and any values ofand VO2assess how the state of decompensation in the system of oxygen transport to the brain and its metabolism.

2. The method according to claim 1, characterized in that the evaluation of the system of transport of oxygen to the brain spend over 8 hours in an unstable state of the patient, after stabilization of 1 times a day, with the formation of a persistent vegetative state or regression of cerebral symptoms until 9-10 points on a scale Glasgow coma monitoring ceased.



 

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