Safety of acute normovolemic haemodilution with hydroxyethyl starch during intracranial surgery

K M Kiran Prasad1, T S Devaragudi, R Christopher

  • 1Department of Neuroanaesthesia, National Institute of Mental Health and Neurosciences, Bangalore, 560029, India.

Neurology India
|February 7, 2001
PubMed

The effect of acute normovolemic haemodilution on haemodynamics, serum osmolality and coagulation parameters was studied in 20 patients undergoing intracranial surgical procedures. After induction of anaesthesia, 740+/-153 ml of blood was collected and the same was replaced with an equal volume of 6% hexaethyl starch. Heart rate (HR), blood pressure (BP), central venous pressure (CVP) and end tidal carbon dioxide tension (Et CO2) were monitored for 45 min. Haemoglobin concentration (Hb), haematocrit (Hct), serum osmolality (Osm), bleeding time (BT), prothrombin time (PT) and platelet count were determined before and 45 min after haemodilution. Hb and Hct were significantly lower following haemodilution (13.1+/-1.8 and 10.3+/-1.7 g/dL for Hb and 38.0+/-4.6%. and 30.1+/-4.5% for Hct). There was no significant change in the HR, BP and Et CO2 throughout the study period. CVP increased marginally from 35 to 45 min but was within normal limits. There was no significant change in serum osmolality, bleeding time and prothrombin time following haemodilution. Platelet count decreased following haemodilution but the values were within normal limits. The brain relaxation, as assessed by a semiquantitative scale, was satisfactory in all cases. None of the patients developed intraoperative brain swelling. In conclusion, acute normovolemic haemodilution with hexaethyl starch is tolerated well haemodynamically. It does not cause changes in serum osmolality which can increase brain oedema. It has no adverse effect on intraoperative haemostasis. It is a safe technique to decrease homologous blood transfusion during intracranial surgery.

Related Concept Videos

Hemodialysis II: Procedure and Complications01:24

Hemodialysis II: Procedure and Complications

DialyzersA hemodialysis (HD) dialyzer is a plastic cartridge containing thousands of parallel hollow fibers, which serve as semipermeable membranes. These fibers are typically made from cellulose-based or other synthetic materials. During HD, blood is pumped into the top of the cartridge and distributed among these fibers. Simultaneously, dialysis fluid, known as dialysate, is introduced into the bottom of the cartridge, bathing the outside of the fibers. Across the semipermeable membrane,...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Hemorrhagic Stroke ll: Pathophysiology01:29

Hemorrhagic Stroke ll: Pathophysiology

A hemorrhagic stroke develops when a cerebral blood vessel ruptures, allowing blood to escape into the surrounding brain tissue, as in intracerebral hemorrhage (ICH), or into the subarachnoid space, as in subarachnoid hemorrhage (SAH). Because the skull is a rigid compartment, the sudden presence of extravascular blood rapidly increases intracranial pressure and compresses adjacent neural structures, leading to immediate tissue injury and impaired cerebral perfusion.Mass Effect and Primary...
Cerebral Edema l: Introduction01:19

Cerebral Edema l: Introduction

Cerebral edema is a pathological increase in brain water content that disrupts intracranial pressure regulation and impairs neurological function. Because the cranial vault is rigid, even modest increases in tissue volume can compromise cerebral perfusion, distort neural structures, and initiate secondary injury. Cerebral edema develops through four principal mechanisms: vasogenic, cytotoxic, interstitial, and ionic.Vasogenic EdemaVasogenic edema arises from disruption of the blood–brain...