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Hematological principles

1. Neurocritical Care Bundle Wasswa Travor Moderator : Dr. Mwanje Arthur

2. Introduction Neurocritical care focuses on intensive care management of patients with life-threatening neurological and neurosurgical illnesses Encompasses conditions like ; massive stroke, bleeding in or around the brain, brain tumors, brain trauma, status epilepticus, nerve and muscle diseases, spinal cord disorders. (Chen et al., 2025) Guided by general principles of assessment and intervention in a systematic manner

3. Airway & Breathing As with any acute illness, expeditious securing of the airway is the main priority. An obstructed airway should be managed immediately, and one can assume that any amount of hypoxia in the injured brain could add further damage to the brain. Endotracheal intubation should be performed in patients who cannot protect their airway, in those who may have aspirated gastric contents, and certainly in those with decreased alertness during which airway obstruction may occur.

4. Depression of the level of consciousness is not an absolute indication for mechanical ventilation. Intubated patients with acute CNS disease are generally able to maintain efficient gas exchange. However, patients with abnormal breathing patterns that result in inadequate oxygen delivery and hypercapnia need to be mechanically ventilated. Noninvasive mechanical ventilation (BiPAP) is a reasonable option in many postoperative patients with marginal oxygenation. In any patient on mechanical ventilation, a “ventilator bundle” is ordered (head elevation 30 degrees; peptic ulcer and venous thromboembolism prophylaxis). Most patients with acute neurosurgical illness can be supported with intermittent mandatory ventilation and pressure support ventilation. Many patients can be quickly transitioned to a continuous positive airway pressure mode if there are few and clear secretions and no pulmonary infection, aspiration, or edema.

5. Early tracheostomy should be considered when prolonged mechanical ventilation is anticipated, but the timing of tracheostomy is controversial. Leads to better patient comfort, more effective tracheal suctioning, and perhaps a decrease in the considerable risk for tracheolaryngeal stenosis from prolonged intubation. Tracheostomy may reduce pulmonary complications and shorten the ICU stay. Goal is to maintain normal partial pressures of oxygen and carbondioxide in blood.

6. About 20% of these patients require mechanical ventilation of which 20–25% will develop acute respiratory distress syndrome (ARDS) (Esteban et al., 2000) Acute brain injury can create issues in lung function and vice versa. This bidirectional brain-lung interaction is supported in experimental models and basic studies in humans, which have shown several neuroinflammatory, autonomic, immunologic, and endocrine pathways.

7. According to the so-called two-stroke model, when acte brain injury occurs, a lung injury associated with systemic inflammation due to a “catecholamine storm” appears i.e. first hit. Subsequently these events can trigger an increase in permeability into the pulmonary capillaries, vasoconstriction in the pulmonary arterioles and recruitment of inflammatory cells in the alveoli i.e. second hit. (Mascia et al., 2011) Hypoxemia and hypercapnia are associated with lung injury and amplify acute brain injury. Both situations reduce cerebral vascular resistance, which consequently raises cerebral blood flow and increases ICP.

8. In patients with ABI, it is fundamental to guarantee an optimal oxygenation to avoid secondary brain injury. It is recommended to target “normoxia” with a partial arterial pressure of oxygen (PaO2) between 80-120 mmHg and or a peripheral oxygen saturation (SpO2) of ≥95% in patients with or without intracranial hypertension . (Robba et al., 2020) In addition, some evidence suggests that hyperoxia is an independent factor associated to greater mortality and outcomes driven by several mechanisms: vasoconstriction of brain arteries, synthesis of reactive oxygen species (ROS) and damage associated molecular patterns (DAMPs). (Vincent et al., 2017)

9. It is recommended to adjust the ventilation to maintain normal levels of arterial pressure of carbon dioxide (PaCO2) between 35 and 45 mmHg. Traditionally, it was considered that patients with ABI (specially population with TBI) should be maintained with hyperventilation; however, this situation can lead to cerebral vasoconstriction that can worsen cerebral tissue hypoxia and ischemia. In a randomized clinical trial conducted by Muizelaar et al., it found that patients with TBI undergoing systematic hyperventilation (PaCO2 25 ± 2 mmHg) had poorer outcomes at 3 and 6 months’ follow-up compared with the normocapnia group (PaCO2 35 ± 2 mmHg). Transient hyperventilation (PaCO2 30–35 mmHg) is only recommended as a rescue maneuver in cases of brain herniation

10. Circulation Optimal blood pressure (BP) management is controversial in neurocritically ill patients due to conflicting concerns of worsening ischemia with decreased BP versus cerebral edema and increased intracranial pressure with elevated BP. Blood pressure (BP) management is essential in neurocritical care settings to ensure adequate cerebral perfusion and prevent secondary brain injury

11. Circulation Hypovolemia is a potential clinical problem in all patients with acute CNS illness. Triggers at least three physiologic pathways—antidiuretic hormone, renin, and norepinephrine—all facilitators of sodium reabsorption, but these mechanisms may not be sufficient. Failure to recognize the inability of patients with depressed consciousness to signal thirst may lead to rapid loss of intravascular volume. In addition, insensible losses associated with fever or emesis are commonly underestimated. Hypovolemia may go unnoticed for some time, until the patient is placed on mechanical ventilation with positive pressure support, which will result in reduction of venous return, decreased cardiac output, and hypotension.

12. Postoperative hypertension is best managed by treatment of pain (mostly fentanyl), hypoxemia, and volume overload, if present. Initial correction of hypovolemia should be done with crystalloids (normal saline). Glucose-containing solutions may precipitate increased lactate production and secondary brain injury. Insensitive losses should be taken into consideration when calculating fluid deficits. Gastrointestinal losses average 250 mL/day, and evaporation of fluid through the skin and lungs accounts for losses of 750 mL/day. Fever increases evaporation and can lead to losses of 500 mL/°C above normal.

13. Indicators of Volume Status in Patients with Acute Neurologic Illness Urinary output of 1 mL/kg/hr Fluid intake of 30 mL/kg/day Fluid balance excess of 750-1000 mL/day Maintenance or a slight increase in body weight Patient with adequate fluid balance should have a hematocrit of less than 55%, an osmolality of less than 350 mOsm, and a serum sodium concentration of less than 150 mEq/L. Any higher values should signal dehydration. Goal is to maintain normal MAP

14. The general formula for cerebral blood flow (CBF) is as follows: CBF = (MAP – ICP) / CVR Since neurons are highly dependent on adequate substrate delivery in order to maintain viability, cerebral blood flow (CBF) is tightly controlled. The brain maintains a constant CBF at approximately 50 mL/100 g/minute despite large changes in BP and CPP. When BP increases, cerebral vessels constrict and CVR increases in order to maintain a constant flow. When BP decreases or ICP increases, the vessels dilate and CVR decreases to keep CBF constant. The cerebral autoregulation is effective in a mean arterial pressure (MAP) range of 50–150 mm Hg in normotensive individuals. (Vivek et al., 2019)

15. Systolic blood pressure plays a very important role in contributing secondary injury cascade after severe traumatic brain injury. As early as 1989, Klauber et al. reported a mortality of 35% in patient admitted with SBP <85 mm Hg, compared with only 6% in patients with a higher SBP. Additionally, hypotension has been shown to correlate with diffuse brain swelling. If autoregulation is not intact, there is dependency on SBP to prevent cerebral ischemia which is the single most important secondary insult. The 4th edition of BRAIN TRAUMA FOUNDATION recommends maintaining SBP >100 mm Hg for age 50–69 years (>110 mm Hg for age 15–49 years) is considered to decrease mortality and improve outcome. Though majority of guidelines target systolic BP, targeting cerebral perfusion pressure (CPP) is more physiological. Brain Trauma Foundation guidelines recommend routine CPP monitoring in severe TBI patients, which is said to decrease 2 weeks mortality. CPP target for survival and favourable outcome is between 60 mm Hg and 70 mm Hg. (Carney et al., 2017)

16. During initial phase of traumatic brain injury, till bleeding is not controlled one should aim for SBP target of >90 mm Hg.

17. During hyperemic phase there is “luxury perfusion” because of increased cerebral blood flow due to vessel dilatation. During this phase one must target for CPP of around 60 mm Hg. Also, during late phase of TBI, there may be vasospastic phase, so you should be targeting slightly higher perfusion pressures by targeting higher SBP and MAP.

18. Disability

19. Temperature Control Fever is a key clinical sign that mostly signals infection. Fever is also associated with poor outcome after ischemic stroke, intracerebral hemorrhage, and aneurysmal subarachnoid hemorrhage, but the pathophysiologic effects of increased brain temperature on neuronal function are not well understood. Fever develops in 25% to 50% of NICU patients. Fifty-two percent of fevers were explained by an infectious etiology, with pulmonary pathology being most predominant. Infectious causes should be aggressively sought (chest radiograph; blood, urine, and sputum cultures), but noninfectious causes of fever may occur and include reaction to blood products, deep venous thrombosis (DVT), drug fever, postsurgical local tissue injury, pulmonary embolism (PE), and central fever with its extreme autonomic storms (episodes of profuse sweating, tachycardia, tachypnea, and bronchial hypersecretion).

20. Initial management of fever includes the administration of acetaminophen, but even high doses may sometimes not be effective. Other measures include environment control, tepid sponging, gastic/urinary lavage, administration of centrally acting pharmacological agents. Goal is to maintain normothermia

21. Targeted temperature management (TTM) is often used in neurocritical care to minimize secondary neurologic injury and improve outcomes. TTM encompasses therapeutic hypothermia, controlled normothermia, and treatment of fever. TTM is best supported by evidence from neonatal hypoxic-ischemic encephalopathy and out-of-hospital cardiac arrest, although it has also been explored in ischemic stroke, traumatic brain injury, and intracranial hemorrhage patients.

22. Fever is often a contributor to secondary injury and is associated with greater morbidity and mortality Active temperature control should continue for as long as the brain is at risk of secondary injury. Continuous monitoring of temperature in patients who are mechanically ventilated is the gold standard, and where continuous monitoring is not possible, at least hourly monitoring is recommended.

23. In the absence of direct measurements, core temperature is the most useful surrogate measure of brain temperature. Other options include axillary & tympanic temperature measurements. Within the core temperature option, discussions centred around oesophageal, bladder, rectal, and intravascular measurements. Bladder and oesophageal were singled out as the favoured core temperature measurements. (Paal et al., 2021)

24. Rectal temperature monitoring was widely regarded as impractical for reasons such as the lag time, a high rate of dislocation, and potential embarrassment for the patient In non-ventilated subjects, and in particular where oesophageal or bladder temperature measurements are not available, tympanic temperature measurement is preferred.

25. The main aims of TTM in a critical care setting, while the brain is at risk, should be maintenance of temperature between 36.0 ° C and 37.5 ° C and prevention of an increase in temperature above 37.5 ° C. Temperature should ideally be centred at 36.5 ° C on the understanding that the maintained temperature will be susceptible to the accuracy of the device and the variability of individual techniques, and that brain temperature can be up to 2 ° C higher than core temperature. The maximum temperature variation that these patients should experience during TTM for normothermia is ideally less than plus or minus 0.5 ° C per hour, and <1 ° C per 24-h period. (Lavinio et al., 2023)

26. Nutritional needs Early feeding of the gut to ensure adequate nutrition is part of daily care. The main goal of nutrition should be to mainatian normal blood glucose levels , preserve muscle mass and provide adequate fluids, minerals, and fats. Caloric needs can be estimated by weight and approximate 25 to 30 kcal/kg per day. The nutritional needs of patients with critical neurological illness should be calculated with the Harris-Benedict formula to obtain the basal energy expenditure (BEE) in calories. The Harris-Benedict equations are based on weight in kilograms, height in centimeters, and age in years. For men, BEE = 66.5 + (13.75 × weight) + (5.003 × height) − (6.775 × age), and for women, BEE = 655.1 + (9.563 × kg) + (1.850 × cm) − (4.676 × age).

27. The integrity of the gut is maintained by enteral feeding and greatly challenged by parenteral nutrition. Gastrostomy placement should be considered in patients with a prolonged need for enteral nutrition because of impaired swallowing mechanisms. Gastrostomy should also be considered if recovery from dysphagia is not anticipated for 2 to 3 weeks. Parenteral nutrition is however still a viable option when enteral feeding is not feasible.

28. Intracranial Pressure Intracranial pressure (ICP) is tightly controlled. According to the Monro-Kellie model, overall intracranial volume is constant because of the rigidity of skull, which does not permit any expansion. An increase in the volume of any component leads to a compensatory decrease in other components or eventual displacement of brain tissue through the tentorial opening or foramen of Magnum and possibly brainstem displacement and loss of brainstem function.

29. Several compensatory mechanisms may prevent this complication. First, CSF may shift from the ventricular or subarachnoid space into the spinal compartment. Second, reduction of intracranial blood volume is achieved by collapse of veins and dural sinuses and by changes in the diameter of cerebral vessels. If the limits of the compensatory mechanisms are exceeded, a minimal increase in intracranial volume will lead to a precipitous rise in ICP.

30. Autoregulation is usually severely impaired in patients with acute neurological injury. Monitoring of ICP is an integral function of neurocritical care.

31. Head position should be neutral to reduce any possible compression of the jugular veins. Head elevation of 30 degrees is considered standard. Patients should be made comfortable, and pain, bladder distention, and agitation should be avoided because these factors might increase ICP. The patient should be maintained in a euvolemic state. Hypovolemia caused by fluid restriction does not have an impact on ICP but may result in hypotension and unnecessary risk to already compromised brain tissue. Hyperventilation is one method of reducing ICP. Hypocapnia causes cerebral vasoconstriction, which in turn reduces cerebral blood flow. This effect is maintained for several hours, after which it becomes ineffective because of compensatory rapid buffering of alkalotic CSF. Aggressive hyperventilation might however decrease cerebral blood flow to levels approaching ischemia. Consequently, hyperventilation should be used only as a bridging measure while other means of ICP control are being instituted.

32. Osmotic diuresis is the mainstay of medical therapy for elevated ICP. The most widely used diuretic agents for the treatment of increased ICP are mannitol and hypertonic saline. The basic mechanism of this intervention is transport of extracellular water to the intravascular space. Failure to respond to osmotic agents might lead to the use of barbiturates. Barbiturates are useful in reducing ICP even in patients resistant to standard medical and surgical therapies.

33. References 1. Mascia L. Acute lung injury in patients with server brain injury: A double hit model . Neurocritical Care. 2011;37:1182-1191 2. Robba C, Poole D, McNett M, et al. Mechanical ventilation in patients with acute brain injury: Recommendations of the European Society of Intensive Care Medicine consensus . Intensive Care Medicine. 2020;46(12):2397-2410 3. Vincent JL, Taccone FS, He X. Harmful effects of hyperoxia in postcardiac arrest, sepsis, traumatic brain injury, or stroke: The importance of individualized oxygen therapy in critically ill patients . Canadian Respiratory Journal. 2017;2017:2834956

34. 4. Carney N, Totten AM, O’Reilly C, Ullman JS, Hawryluk GW, Bell MJ, et al. Guidelines for the Management of severe traumatic Brain injury, Fourth edition. Neurosurgery. 2017 ;80: 6–15 5. Vivek J., Jitendra C., Rahul P. (2019). Blood Pressure Target in Acute Brain Injury . Indian Journal of Critical Care Medicine: 10.5005/jp-journals-10071-2319 6.Paal P., Pasquier M., Darocha T. Accidental hypothermia : 2021 update. Int J Environ Res Public Health. 2022; 19:501

35. 7. Lavinio A. Targeted temperature management in patients with intracerebral haemorrhage, subarachnoid haemorrhage, or acute ischaemic stroke: updated consensus guideline recommendations by the Neuroprotective Therapy Consensus Review (NTCR) group . British Journal of Anaesthesia, Volume 131, Issue 2, 294 - 301

36. Thank you