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Tokmakov K.A., Gorbachev V.I., Unzhakov V.V., Gorbacheva S.М.
Russian Medical Academy of Continuous
Professional Education, Irkutsk, Russia,
Regional
Clinical Hospital No.2, Khabarovsk, Russia
Institute of Postgraduate Education for Healthcare Specialists,
Khabarovsk, Russia
A CASE OF SUCCESSFUL CARRYING OUT THE GENERAL NONINVASIVE HYPOTHERMIA IN NEUROGENIC FEVER IN THE PATIENT WITH A SEVERE CRANIOCEREBERAL INJURY
Increasing body temperature is a quite common symptom
in critically ill patients. According to the literature data, 26-70 % of adult
patients have the elevated body temperature in ICU [1-4]. The incidence is even
higher among patients of neurocritical unit [5]. So, the body temperature >
37.5°C is noted in 60 % of patients with traumatic brain injury (TBI) in ICU
[6]. The causes of elevated body temperature are different. All causes can be
divided into two groups: infectious and non-infectious. The patients with
primary cerebral injury may have the so called centrogenous hyperthermic
response (neurogenic fever in English literature) as one of the non-infectious
causes of fever (in 4-37 % of cases with traumatic brain injury) [7]. The
pathogenesis of centrogenous hyperthermia is not studied enough [8]. A
cadaveric study showed that hypothalamus injuries were in 42.5 % of TBI cases
in combination with hyperthermia [9].
There are some conclusive evidences that the
hyperthermic response increases the possibility of lethal outcome in patients
with cerebral injury [10-13]. Therefore, the necessity of correcting the elevated
body temperature does not raise doubts. However the studies showed that
centrogenous hyperthermic responses are more or less resistant to conventional
pharmacological therapy [9, 14]. Only 7 % of the patients with TBI demonstrated
the decreasing body temperature at the background of antipyretics
administration [15].
There is not a uniform technique for correcting
centrogenous hyperthermic responses. Considering the fact that the centrogenous
hyperthermic response is the exclusion diagnosis, then early differential
diagnostics and appropriate intensive care of this condition are necessary for
patients with traumatic brain injury and improving clinical outcomes in such
patients.
The presented case of
treatment corresponded to the standards of the ethical committee of Institute
of Postgraduate Education for Healthcare Specialists and Helsinki Declare of
World Medical Association.
The patient, age of 20, was transported by the
emergency medical team to the admission unit of Khabarovsk City Clinical Hospital
No.2. The patients had some complaints for headache, nausea and vomiting. From
the disease history it was known that the patient suffered from a knife injury
to the head after quarrel with his fellow student. The life history and the
general examination did not find any significant notes.
The neurological status: clear consciousness, GCS =
15, the pupils were equal, the photoreaction was weak to the right. Right-sided
ptosis, depressed corneal reflex to the right. The
face
was
asymmetrical.
No
paresis
in
the
extremities.
Meningeal signs including rigidity
of occipital muscles up to 4 cm. Some pathological plantar signs were on both sides.
Tendon reflexes were equal and weak. No signs of urinary incontinence.
After the local examination, the neurosurgeon of the
admission unit made a record: “a lineal skin incision of 3 cm in the zygomatic
region to the right, with a knife penetrating up to the deep of 10 cm”.
Cerebral computer tomography identified a lamellar
subdural hematoma to the right, a knife with its blade penetrating the pterygopalatine
fossa, with penetration upwards, through the basis of the middle cranial fossa;
the knife tip is near the Turkish saddle (Fig. 1).
Figure 1. Cerebral CT on the day of admission
(reconstruction)
The diagnosis was made on the basis of the primary
examination: “Opened penetrating TBI, severe brain contusion, stab incised
wound of the head with the middle cranial fossa damage”.
After making the diagnosis, the patient was
transported to the surgery room. Decompressive cranial trepanation was
conducted in the right frontotemporal region during the surgery. Acute subdural
hematoma (about 80 ml) was removed. The brain was moderately edematous (with
pulsation) in the region of the removed hematoma. The approach to the cavernous
sinus was made. The knife blade was found there. Arterial and venous bleeding
was in the region of the sinus injury. The injury to the cavernous region of
the internal carotid artery (ICA) was suspected. The tourniquet was applied to ICA.
The knife was removed from the wound under the visual control of the sinus. Intensive
arterial bleeding initiated from the sinus defect. Later ICA was ligated, and
bleeding intensity significantly decreased, but it was not arrested completely.
There was an unsuccessful attempt of packing for the sinus defect. Successful packing
was performed later: plastics for sinus wall with use of medical felt, with
further ICA opening. The time of ICA cross-clamping was two times per 5 minutes
with 3 minutes intervals. Bleeding was arrested. The total intrasurgical blood loss
was about 500 ml. The plastic surgery of the skull base was performed with use
of Tachocomba plate. The general duration of the surgery was 4 hours. During
the surgery, hemotransfusion for correcting volume of circulating red blood
cells (566 ml) was without complications. The anesthesia included total
intravenous anesthesia with tracheal intubation. The anesthesia components were
the main anesthetic (propofol), the analgetic (fentanyl), myorelaxant (pipecuronium
bromide). The hemodynamically stable course of anesthesia was observed with
short time elevation of arterial pressure (AP) and increasing heart rate (HR)
at the stage of removal of the foreign body. After the surgery, the patient was
transported to the intensive care unit.
Cerebral CT was conducted in the early postsurgical
period for postsurgical controlling. No hematomas were found. There were some
air bubbles and minimal hemorrhagic impregnation in the right middle cranial
fossa. The course of the cerebral vessels and their caliber were without
changes. There were not any signs of carotid cavernous inosculation. The region
of the bone defect included the muscle saturated with bleed, with moderate
extensive influence on the right frontal and temporal lobes. The median
structures displaced by 2 mm leftwards. The
subarachnoidal
spaces
were
without
changes
(Fig.
2).
Figure 2. Cerebral CT on the second day after removal of a
foreign body
The patient’ condition was critical and stable during
two days after the surgical management. The condition severity was determined
by cerebral insufficiency.
The neurological status: GCS = 6. Pupils D > S. Photoreactions
were persistent. The face was symmetrical. No meningeal signs. Equal tendon reflexes. No pathologic plantar signs and paresis. Sensitivity
was
normal.
Vegetative
disorders
were
absent.
The hemodynamics was stable. The synchronization
with
the
artificial
lung
ventilation
device
was
performed.
Normothermia persisted. The
laboratory values were within the normal range.
Some negative trends were observed on the third day.
At the background of persistent coma, the patient demonstrated febrile
hyperthermia, sinus tachycardia, arterial hypertension. The patient was
desynchronized with the ALV device. It was accompanied by hyperventilation. Sibazon infusion (15-20 mg/h) was initiated for
correcting the changes. Cerebral CT was conducted over time.
On the third day after hospital admission, cerebral CT
found that the cerebral structures had displaced by 3 mm leftwards. There were
no hematomas. The small amount of the air was identified in the middle cranial
fossa to the right. Some remains of the lamellar subdural hematoma were in the
right parietal region. The lateral ventricles were narrowed. The embracing
cistern was deformed. The fourth ventricle was narrowed. Bilateral semispheric
edema was found (Fig. 3).
Figure 3. Cerebral CT on the third day
The complex of the diagnostic procedures for
identifying a possible cause of fever was used owing to development of the
hyperthermic response with persistence to the antipyretic (metamizole sodium)
and more than 24 hours duration at the level of febrile and pyretic values, the
non-stable condition with such clinical manifestation as sinus tachycardia,
arterial hypertension, desynchronization with ALV device with development of
hyperventilation at the background of consciousness depression with transition
to coma. First of all, the diagnosis of systemic inflammatory response syndrome
(febrile hyperthermia with tachycardia and hyperventilation) was made,
procalcitonin test was made (negative result), and blood culturing for
sterility (the result was sterility) was carried out. For excluding possible
bronchopulmonary infectious pathology, the chest radiography (frontal view, no
pathology), diagnostic fiberoptic bronchoscopy (sputum with mucous pattern, no
signs of endobronchitis). Cerebrospinal fluid puncture was made (clear and
clean liquor).
The antibiotic therapy was initiated simultaneously
with the diagnostic procedures (ceftriaxone, 1 g, 2 times per day).
Pharmacological antipyretic therapy was continued (metamizole sodium).
Considering persistent hyperthermia at the background
of antibacterial therapy and absent reliable data after examinations of the
infectious cases of fever, the diagnostic search was redirected to the
non-infectious causes. The pharmaceutical and allergic anamnesis was collected
with help of the patient’s mother. As result, a possible source of hyperthermia
was not found. The patient had not any signs of drug fever such as relative
bradycardia, skin rash, eosinophilia. The ultrasonic examination of the lower
extremity veins was carried out. Thrombosis
was
excluded.
The diagnosis “centrogenous hyperthermic response” was
made after exclusion of possible infectious and non-infectious causes of fever,
its persistence during antibiotic therapy and non-efficient traditional
antipyretic.
Non-invasive hypothermia with use of controlled
hyper/hypothermia and the active cooling technology Blanketrol II CZN with
water basis and the microprocessor control and patient feedback was initiated
on the fourth day for correcting centrogenous hyperthermic response. Sibazon
sedation (15-20 mg/h) was continued for preventing and correcting shivering.
The targeted body temperature of 35 °C was achieved within two hours after
initiation of the procedure. The temperature was measured in the axillary
cavity.
Cerebral CT was conducted on the fifth day. There were
some positive trends in comparison with the previous CT examination on the
third day in ICU. Semispheric edema decreased. The middle structures shifter by
2 mm leftwards. The lateral ventricles are normally visualized. The embracing cistern
and the fourth ventricle are deformed and sharply narrowed (Fig. 4).
Figure 4. Cerebral CT on the fifth day
Considering the clinical data, the complex ultrasonic examination of the cerebral brachiocephalic vessels was carried out for identification of possible causes of the centrogenous hyperthermic response, despite of positive time course according to CT examination. A cerebral angiospasm was not found (the table).
Table. Complex ultrasonic examination of cerebral brachiocephalic vessels on the fifth day
|
Artery |
To the right |
To the left |
||
|
LBFV max/min cm/sec |
TPRI |
LBFV max/min cm/sec |
TPRI |
|
|
ICA |
80/38 |
0.51 |
65/37 |
0.42 |
|
MCA |
234/119 |
0.49 |
140/66 |
0.53 |
|
ACA |
168/82 |
0.51 |
100/48 |
0.51 |
|
PCA |
197/72 |
0.48 |
73/23 |
0.68 |
|
Lindegard’s index |
2.9 |
2.2 |
||
Note: ICA – internal carotid artery, MCA – medial cerebral artery, ACA – anterior cerebral artery, PCA – posterior cerebral artery, LBFV – linear blood flow velocity, TPRI – total peripheral resistance index.
The phase of targeted temperature maintenance (35 °C)
lasted for 4 days. The interesting fact is temperature variability +/-1 ° in
comparison with the targeted value. The long term myorelaxant was used for
correcting shivering within a day.
Cerebral magnetic resonance imaging was conducted.
There was a focus of abnormal MR signal in the region of subcortical nuclei.
The signal was hyperintensive in the mode of diffusion weighted imaging (DWI).
It could correspond to lacunary stroke (Fig. 5).
Figure 5. Cerebral MRI on the seventh day after admission
Therefore, cerebral MRI examination identified some
possible structural cases of the centrogenous hyperthermic response.
The phase of maintaining the controlled hypothermia
lasted up to 19 day of ICU stay. Owing to the stable condition of the patient,
the controlled hypothermia was attempted to stop two times on the days 12 and
16 after the surgery (on the days 8 and 12 after initiation of controlled
hypothermia). The phase of warming was conducted with the rate of 0.1 °C within
an hour with reaching 36.6 °C. It was accompanied by discontinuation of sibazon
sedation. But owing to appearance of febrile hyperthermia, controlled general
non-invasive hypothermia was restarted (Fig. 6).
Figure 6. Temperature changes during ICU stay
Tracheostomy was carried out on 7th day from the
injury moment owing to need for long term respiratory support and continuous
sanitation of the tracheobronchial tree.
One should notice that polyuria developed from 6th day
of ICU stay (and from 3rd day after initiation of controlled hypothermia), and
it was considered as a result of hypothalamus injury. After prescribing desmopressin
and selecting the dosage, the diuresis rate normalized by 14th day. It is
interesting that the patients demonstrated the increasing diuresis rate and
febrile hyperthermia, despite of continuous administration of titrate dose of
desmopressin, on 17th day after withholding the controlled hypothermia. The
diuresis
rate
restored
after
restarting
hardware
hypothermia
(Fig.
7).
Figure 7. Diuresis time course
The plasma levels of К+ and Na+ electrolytes, urea, creatinine,
bilirubin and glucose remained within the normal range during controlled
hypothermia.
If an infectious source of hyperthermia was not
identified at the moment of initiation of controlled hypothermia, then, on the
day 13, the general blood analysis showed leukocytosis with leftward shift to myelocytes,
and the chest X-ray examination showed the decreasing pneumatitization by the
infiltration type in the right region in the plane of the lower lobe, resulting
in confirming the diagnosis “ventilator-associated right-sided lower lobe
pneumonia”. The results of sputum inoculation showed that Acinetobacter baumannii
was a possible causative agent. After prescription of imipenem and cilastatin (Acinetobacter
baumannii was sensitive to them), the positive time course of the laboratory
and instrumental values was observed. There were not any ventilation disorders
during the follow-up.
Cerebral CT was conducted on 26th day of hospital
stay. The cranial trepanation was carried out on the right side and showed some
hydromes in the trepanation field (subdurally, the layer up to 1.2 cm, the
volume up to 40 ml), a subcutaneous hydrome (the layer up to 1.4 ml). Some
cystic changes were in the base of the temporal lobe to the right. The signs of
atrophy (extension of subarachnoidal spaces) were in the right hemisphere. The
middle structures were not displaced. There were not any mass lesions or
hematomas. The ventricles were easily extended, the basal cisterns with
satisfactory differentiation (Fig. 8).
Figure 8. Cerebral CT on the 26th day of hospital stay
The general controlled hypothermia and sibazon
infusion were arrested on 29th day of ICU stay. The body temperature did not
exceed the subfebrile values during those and subsequent days in ICU.
The consciousness restored
on 34th day. The independent breathing was on 36th day. The patient was
transported to the neurosurgery unit on 39th day, where decanulation was performed.
The patient was discharged for outpatient treatment on 47th day of hospital
stay. His condition was satisfactory. The final clinical diagnosis: “Severe opened penetrating traumatic brain injury;
severe brain contusion; penetrating stab wound of the middle cranial fossa; incised
wound of the right zygomatic region; syndromes: psychoorganic, vestibular atactic,
general cerebral; traumatic damage of the right oculomotor nerve”.
CONCLUSION
The use of general controlled non-invasive hypothermia
in complex management of the centrogenous hyperthermic response in patients
with severe traumatic brain injury is an efficient technique of decreasing body
temperature, considering the fact that the conventional techniques of fever
arrest has the low efficiency in this case. The results of neurovisualizing
techniques showed that the technique of controlled hypothermia promoted the
decrease in intensity of cerebral edema.
The technique was safe. It
was supported by the results of the laboratory and clinical examinations.
However development of pneumonia during treatment at the background of the
controlled hypothermia system suggests that for further use of the technique,
the special attention should be given to prevention of hospital infections and
researching whether this technique is a predisposing factor of the infections,
for example, by means of depressing the immune response of the patient.
Information about financing and conflict of interests:
The study was conducted without sponsorship.
The
authors declare the absence of clear and potential conflicts of interests
relating to the publication of this article.
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