top of page
Post: Blog2_Post

ICP Considerations For Transport Providers

Transport Management of the Intracerebral Hemorrhage Patient

Traumatic Brain (TBI) Injury is the most common trauma related cause of death and disability. These injuries are usually characterized as primary (immediate damage from mechanism fall, MVAs, assault, GSW, explosions) and secondary (insults occurring after the initial impact such as ischemia, hypoxia, reperfusion, or infection).

TBIs usually refer to the epidural, subdural, and subarachnoid hemorrhages. In contrast to this, there are intracerebral hemorrhages (ICH) that include intraventricular and intraparynchymal bleeds of which the majority are due to severe hypertension (inadequately treated or undetected chronic hypertension) and are localize to the cerebellum, brainstem and the midbrain. These can be also be aneurysmal or from tumors. Blood pressure from intracerebral hemorrhage often becomes elevated, frequently reaching very high levels and is a predictor of outcome. Hypertensive responses to other factors are thus exaggerated and additive because of impaired parasympathetic activity and baroreceptor sensitivity in patient with ICH.

Since the insult has already occurred for these patents, it is up to us, in the transport environment, to make sure that we prevent them from the secondary injuries and thus do no harm. There is an excellent resource with guidelines that have been updated as of 2016 by the Brain Trauma Foundation (BTF). This resource can be found here:

Here is what to consider and management pearls for the TBI and ICH patient:

AVOID HYPOXIA Hypoxemia and Hypotension have been considerable factors in poor prognosis in TBI patients, and all reasonable efforts should be made to avoid this. We can do this by monitoring for the presence of apnea, disorganized breathing, cyanosis, pulse ox saturations < 90%, or PaO2 <60 mmHg and by correcting it.

Pulse ox and ETCO2 should be monitored frequently, if not continuously, in these patients.

Hypoxemia should be avoided and corrected immediately upon identification.

Place your patient on O2 if needed. Take control of their airway if they have disorganized breathing or are gargling. Sometimes simple positioning can help. Elevate the head of the bed 30-45 degrees and make sure the neck is in a neutral position.

If the patient requires intubation due to loss of airway, confirmation with ETCO2 is key to avoid hypoxia or a missed goosed tube.

Make sure to pre-oxygenate well, have appropriate equipment with backup method, and avoid hypoxia with intubation.

Consider using Rocuronium as your paralytic because it is a non-depolarizing muscle blocker.

Patients should be maintained with normal breathing rates (ETCO2 35-40 mmHg) and hyperventilation ETCO2 < 35) should be avoided. If the patient is with signs of acute herniation (pupils blown or unequal, disorganized breathing, and posturing) you may consider short term increase in respiratory rate. This type of hyperventilation should be discontinued as soon as signs of herniation resolve and this should only be used in short duration.

Ventilation strategies per BTF2: (Level IIB = based in low quality body of evidence) Hyperventilation is not recommended. Previous recommendations by the 3rd Edition were not supported by evidence. Routine hyperventilation is not recommended for patients with TBI as vasoconstriction may decrease cerebral perfusion pressure and worsen secondary injuries. Be cognizant of when the patient is being oxygenated and ventilated via bag-valve-mask by hand, as sometimes the provided respiratory rate is often much too high which can lead to inadvertent hyperventilation and hypocarbia. Care should be taken to monitor the rate of respiration/ventilation either by ventilator or when hand-bagging a patient and to follow blood gasses for measurement of PaO2 and PaCO2.

AVOID HYPOTENSION Avoid hypotension by making sure to recheck vitals frequently (q5min), have appropriate sized BP cuff, and have IV access available (2 PIV preferred yet do not delay transport for 2nd IV). If SBP < 90 mmHg, consider fluids. Each single hypotensive episode with a MAP <85 mmHg in a TBI patient doubles the mortality and morbidity.

Crystalloid administration will not aggravate cerebral edema as it is much more important to avoid hypotension in these patients.

Blood Pressure Monitoring per BTF2: (Level III = low quality of indirect evidence) Maintain

SBP > 100mmHg for patients 50-69 yo

SBP > 110 mmHg or above for patients 15-49 yo or > 70 yo

Combating hypertension may be considered to decrease mortality and improve outcomes.

AVOID HYPERTENSION Simple maneuvers that may help are elevating the head of bed to 30 degrees or using a reverse Trendelenburg. Consider keeping the patients head and neck in a neutral positive to avoid compression on the jugular veins. Providing analgesia may help reduce BP as well.

The goal is to keep SBP <160 mmHg to prevent rebleeding. Although further reduction of SBP to < 140 has not been shown to improve clinical outcomes, it is common practice to lower SBP per previous recommendations. Hypertension should be treated when cerebral perfusion pressure (CPP) >120 mmHg or intracranial pressure (ICP) >20 mmHg.

Goal is to maintain CPP between 60-70 mmHg


In the absence of invasive monitoring your neurologic exam will be the best indication of increasing ICP.

If you are one of those people that love trials with cool names then this is for you… According to

The ICH ADAPT13, INTERACT 114 and INTERACT 215 trials have demonstrated how lowering SBP to < 140-150mmHg was safe, perihematomal blood flow was preserved, and did not increase mortality or rates of dependency or neurological deterioration when compared to standard treatment control groups ~ SBP <180.

However, only INTERACT215 could demonstrate a tendency (non-significant) towards improved functional recovery with intensive BP lowering.

Sakamoto et al. in the in the SAMURAI16 study, reviewed 211 patients with ICH and hypertension with SBP > 180 mmHg who had nicardipine to achieve SBP < 160 mm Hg. The authors noted how functional 3 month outcomes were best in patients where SBP < 130 was achieved.

Medications to consider to lower BP include these titratable medications to target SBP <160 and MAP <110 (Class IB and IIC recommendations respectively): (Recommendations from PressorDex®, 3rd Ed.)

Nicardipine -Infusion: 5mg/hr, titrate by 2.5 mg/hr q5-15min -Max: 15 mg/hr; onset: 1-2 min, Duration: 40min

Clevidipine -Infusion: 1-2mg/hr, titrate by doubling rate q1-2min; one approaching goal reduce adjustment to 1-2 mg/hr q 5-10 min; Max 21mg/hr

Labetolol -Loading dose: 10-20mg IV, double dose at 10 min intervals to max of 300mg-Infusion: 2-8mg/min, titrate by 0.5 mg/min q10min -Max: 8mg/min; Onset 2-5min; Duration: 2-4hr

Enalaprilat: (Vasotec®) -Initial dose: 1.25 mg IV over 5 min, titrated up to 5mg/dose q6hr -If receiving diuretic: 0.625mg IV over 5min, repeat dose if inadequate in 1hr and increase to 1.25mg IV q6hrs

Hydralazine: Is unpredictable and there is no evidence for its use in SAH.

Hyperosmolar therapy per BTF2:


Recommendations are not supported by evidence yet previously stated to use mannitol (osmotic diuretic) for control of raised ICP at doses of 0.25 to 1 g/kg while avoiding arterial hypotension (SBP<90). So make sure you can replace the volume that the patient will most likely lose after you had made them pee it out!

For increased intracranial pressure withbsigns of herniation consider the use of the following meds: (Recommendations from PressorDex®, 3rd Ed.)

Hypertonic Saline (3%): 250mL (3mL/kg) infused wide open or over 20min, can repeat for max dose 500mL preferably given through central line.

Hypertonic Saline (7.5%): 250mL (2mL/kg) IV bolus preferable through central line

Hypertonic saline (23.4%): 30mL infused over 10min via central line

Mannitol (20%): -Initial dose: 1g/kg IV bolus -May repeat 0.5-1g/kg IV PRN q6-8 hrs for increased ICP so long as serum Osm < 320

Sodium Bicarbonate (8.4%): (contains hypertonic saline) -Infuse 85mL of 8.4% NaHCO3 over 30 min.

There is data to support the use of mannitol in response to herniation if the provider has the ability to provide high fluid volume compensation for ensuing urine losses.

Mannitol serves as a temporizing measure in patients with imminent herniation but it has a limited duration of action and does not provide definitive treatment of intracranial hypertension. Any patient requiring mannitol should receive rapid neuroimaging (CT scan) and prompt re-evaluation by a neurosurgeon for possible surgical decompression.

Look at the Sodium level (Na+ found in the CMP or BMP) in the labs. If the patient is hyponatremic (Na < 135), then limit free water intake. If herniating and have a significantly low sodium (Na <120) then consider hypertonic saline use. Avoid correcting serum sodium more than 10-12mmol/L in 24hrs to avoid osmotic demyelination (aka locked in syndrome).

I highly recommend that anyone working in the critical care environment, Medic, RN, & Physician all get the Pressordex® from EMRA. This is one of the things I always have in my pocket when working. You can get it here:

Cynthia Griffin DO, NRP Board Certified Emergency Medicine Physician, Flight Physician for UW Medflight, Madison & Mineral Point, WI Community ED Physician at St. Agnes, Fond du Lac, WI

References: Prehospital guidelines from the Brain Trauma Foundation can also be found at

The Brain Trauma Foundation also has a manual with guidelines for the Field management of Combat Related Head Trauma which can be accessed at although this appears to have been published in 2005.

⦁ Harwood-Nuss' Clinical Practice of Emergency Medicine (Clinical Practice of Emergency Medicine Fifth Edition 2010 p 157 ⦁ Carney N, Totten A M, O’Reilly C, et al. Guidelines for the Management of Severe Traumatic Brain Injury. Brain Trauma Foundation. Published September 2016. Accessed 12-20-2017 ⦁ Greenwood, John C. PressorDex®, 3rd Ed. EMRA. 2017 ⦁ Accessed 12-20-2017 ⦁ Accessed 12-20-2017 ⦁ Accessed 12-20-2017 ⦁ Accessed 12-20-2017⦁ &⦁ sid=97ec7053-d0bf-464b-9941-8273405294a5%40sessionmgr4008 Accessed 12-20-2017 ⦁ Accessed 12-20-2017⦁ b⦁ med/27178479 Accessed 12-20-2017 ⦁ Teasdale G, Jennett B. Assessment of coma and impaired consciousness: a practical scale. Lancet. 1974; 2:81-84. ⦁ Accessed 12-20-2017 Accessed 12-20-2017 ⦁ Anderson CS, Huang Y, Arima H, et al. Effects of early intensive blood pressure-lowering treatment on the growth of hematoma and perihematomal edema in acute intracerebral hemorrhage: the Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage Trial (INTERACT). Stroke 2010;41:307-312 Accessed 12-20-2017 ⦁ Qureshi AI, Palesch YY, Martin R, et al. Interpretation and implementation of Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial (INTERACT II). J Vasc Interv Neurol 2014;7:34-40 Accessed 12-20-2017 Accessed 12-20-2017 Accessed 12-20-2017 ⦁ Zhang, Yonghong Reilly, Kathleen H Tong, Weijun Xu, Tan Chen, Jing Bazzano, Lydia A Qiao, Dawei Ju, Zhong Chen, Chung-Shiuan He, Jiang. Blood pressure and clinical outcome among patients with acute stroke in Inner Mongolia, China. Journal of hypertension. , 2008, Vol.26(7), p.1446-1452 ⦁ Qureshi AI1. The importance of acute hypertensive response in ICH. Stroke. 2013 Jun;44(6 Suppl 1):S67-9. doi: 10.1161/STROKEAHA.111.000758. ⦁ Robinson TG, James M, Youde J, Panerai R, Potter J. Cardiac baroreceptor sensitivity is impaired after acute stroke. Stroke. 1997;28:1671–1676. ⦁ accessed 12-21-2-017

bottom of page