In this post I link to and excerpt from Guidelines for the Acute Treatment of Cerebral Edema in Neurocritical Care Patients [PubMed Abstract] [Full Text HTML] [Full Text PDF]. Neurocrit Care. 2020 Jun;32(3):647-666.
Here are excerpts:
Background: Acute treatment of cerebral edema and elevated intracranial pressure is a common issue in patients with neurological injury. Practical recommendations regarding selection and monitoring of therapies for initial management of cerebral edema for optimal eficacy and safety are generally lacking. This guideline evaluates the role of hyperosmolar agents (mannitol, HTS), corticosteroids, and selected non-pharmacologic therapies in the acute treatment of cerebral edema. Clinicians must be able to select appropriate therapies for initial cerebral edema management based on available evidence while balancing eficacy and safety.
Methods: The Neurocritical Care Society recruited experts in neurocritical care, nursing, and pharmacy to create a
panel in 2017. The group generated 16 clinical questions related to initial management of cerebral edema in various neurological insults using the PICO format. A research librarian executed a comprehensive literature search through July 2018. The panel screened the identified articles for inclusion related to each specific PICO question and abstracted necessary information for pertinent publications. The panel used GRADE methodology to categorize the quality of evidence as high, moderate, low, or very low based on their confidence that the findings of each publication approximate the true effect of the therapy.
Results: The panel generated recommendations regarding initial management of cerebral edema in neurocritical
care patients with subarachnoid hemorrhage, traumatic brain injury, acute ischemic stroke, intracerebral hemorrhage,
bacterial meningitis, and hepatic encephalopathy.
Conclusion: The available evidence suggests hyperosmolar therapy may be helpful in reducing ICP elevations or cerebral edema in patients with SAH, TBI, AIS, ICH, and HE, although neurological outcomes do not appear to be affected. Corticosteroids appear to be helpful in reducing cerebral edema in patients with bacterial meningitis, but not ICH.
Differences in therapeutic response and safety may exist between HTS and mannitol. The use of these agents in these
critical clinical situations merits close monitoring for adverse efects. There is a dire need for high-quality research to
better inform clinicians of the best options for individualized care of patients with cerebral edema.
Keywords: Intracranial pressure, Neurocritical care, Osmotherapy, Hyperventilation, Hypertonic, Mannitol
Cerebral edema is a non-specific pathological swelling
of the brain that may develop in a focal or diffuse pattern after any type of neurological injury. The underlying cause of this brain swelling is highly variable and relates to multiple physiological cellular changes. The simplest description of cerebral edema is an accumulation of excessive fluid within either brain cells or extracellular spaces. Cerebral edema can be secondary to disruption of the blood brain barrier, local inflammation, vascular changes, or altered cellular metabolism. The identification and treatment of cerebral edema is central to the management of critical intracranial pathologies.
It should be emphasized that the recommendations
in this guideline are based on available medical literature, which may not reflect all aspects of clinical expertise and
The Guidelines are divided into:
Treatment of Cerebral Edema in Patients with Subarachnoid Hemorrhage
Treatment of Cerebral Edema in Patients with Traumatic Brain Injury*
Treatment of Cerebral Edema in Patients with Acute
Treatment of Cerebral Edema in Patients with Intracerebral Hemorrhage
Recommendations for Corticosteroids in Patients
with Intracerebral Hemorrhage
Treatment of Cerebral Edema in Patients with Bacterial Meningitis
Treatment of Cerebral Edema in Patients with Hepatic
Hyperosmolar Therapy Safety and Infusion Considerations
In patients receiving mannitol, does osmolarity or
osmolar gap best predict the likelihood for AKI?
In patients receiving hypertonic sodium solutions,
does the serum sodium concentration best predict
toxicity [AKI, unwanted acidosis] compared to the
serum chloride concentration?
Recommendations for Assessing the Risk of Renal Injury After Mannitol Administration
Recommendations for Assessing the Risk of Toxicity (Acute Kidney Injury or Unwanted Acidosis) After Hypertonic Sodium Solution Administration
Recommendations for the Optimal Administration Method of Hypertonic Sodium Solution
Non‑pharmacologic Treatment of Cerebral Edema
and Elevated Intracranial Pressure
In patients with cerebral edema, how do non pharmacological interventions compare to pharmacological interventions for reduction of cerebral edema?
1. We suggest that elevating the head of the bed to 30
degrees (but no greater than 45 degrees) be used as a beneficial adjunct to reduce intracranial pressure (conditional recommendation, very low-quality evidence).
2. We recommend that brief episodes of hyperventilation can be used for patients with acute elevations in
intracranial pressure (strong recommendation, very
Rationale: In making this recommendation, the panel rated the quality of available evidence was very low. However, a strong recommendation was felt to be appropriate given the extensive amount of practical experience with this therapeutic strategy. Clinicians should be mindful of the limitations of acute hyperventilation related to cerebral blood flow and the extent of PaCO2 reduction. Clinicians should also maintain careful awareness of the duration of therapy to avoid deleterious changes in cerebral perfusion.
3. We suggest that the use of CSF diversion be considered as a beneficial adjunct to reduce intracranial pressure (conditional recommendation, very low quality evidence).
4. While non-pharmacological interventions may be
effective for acute elevations in intracranial pressure,
there is insuficient evidence that non-pharmacological interventions are effective for the treatment of any specific physiological changes that produce brain swelling related to cerebral edema.
Other non-pharmacologic therapies such as surgical decompression and therapeutic hypothermia were not included, as they are adequately addressed by other guidelines*. The overall quality of evidence was very low (Table 14).