Free On-line Access

SPCI - Sociedade Portuguesa de Cuidados Intensivos

Revista Brasileira de Terapia Intensiva

AMIB - Associação de Medicina Intensiva Brasileira


ISSN: 0103-507X
Online ISSN: 1982-4335

Ícone Fechar

How to Cite


Lucena AF, Tibúrcio RV, Vasconcelos GC, Ximenes JDA, Cristino Filho G, Graça RV. Lesões cerebrais agudas e sua influência sobre a motilidade gastrintestinal. Rev Bras Ter Intensiva. 2011;23(1):96-103



Review Article

Influence of acute brain injuries on gut motility

Lesões cerebrais agudas e sua influência sobre a motilidade gastrintestinal

Adson Freitas de LucenaI, Rachel Vasconcelos TibúrcioII, Gregório Carolino VasconcelosIII, José Daylton Araújo XimenesIV, Gerardo Cristino FilhoV, Ronaldo Vasconcelos da GraçaVI

IService of Neurology of Hospital Geral de Fortaleza - HGF - Fortaleza(CE), Brazil
IIMedical Graduation Course of Faculdade de Medicina de Sobral -UFC - Sobral (CE), Brazil
IIIService of Anesthesiology of Hospital Geral de Fortaleza - Fortaleza (CE),Brazil
IVService of Surgery of Hospital Waldemar de Alcântra - Fortaleza (CE),Brazil
VDiscipline of Neuroanatomy and Neurology/Neurosurgery of Faculdade de Medicina de Sobral - UFC - Sobral(CE), Brazil
VIDiscipline of Human Physiology of Faculdade de Medicina de Sobral -UFC - Sobral (CE), Brazil

Conflicts of interest: None.

Submitted on September 3, 2010
Accepted on February 7, 2011

Corresponding author:

Adson Freitas de Lucena
Hospital Geral de Fortaleza - Serviço de Neurologia
Rua Ávila Goulard, 900 - Bairro Papicu Zip Code: 60175-295- Fortaleza (CE), Brazil
Phone: +55 85 3101-7090
E-mail: [email protected]



Subarachnoid hemorrhage can increase intracranial pressure, causing significant morbidity. Acute gastric dilation and delayed gastric emptying are commonly seen in patients with intracranial hypertension, and correction of these gastric abnormalities can facilitate the recovery of patients with brain injuries. We conducted a literature review of both national and international health sciences medical journals and electronic libraries spanning the last twenty-eight years and focused on the brain, gut motility and gastric emptying functional axis either in experimental animal models of brain injury or patients with acute cerebral injuries. Decreased parasympathetic tonus is a potential cause of intracranial hypertension-related food intolerance. Changes in gastrointestinal transit after a brain injury follow a biphasic pattern: an initial phase of accelerated gastric emptying and a late stage of intestinal lethargy. Changes in the physiology underlying gut motility may be essential for homeostatic stabilization in hemodynamically unstable patients. Research studies are necessary to understand the difficult management of intensive care patients with intracranial hypertension secondary to subarachnoid hemorrhages resulting from traumatic brain injuries or rupture of a cerebral aneurysm. Increased intracranial pressure induces massive increases in sympathetic activity, which is responsible for many of the peripheral systemic and gastrointestinal symptoms. Brain injuries leading to significant increases in intracranial pressure result in delayed gastrointestinal emptying due to autonomic nervous system changes.

Keywords: Brain, Intracranial hypertension, Gastric emptying, Gastrointestinal motility




Cerebral parenchyma (80% of the total volume), cerebrospinal fluid (CSF) (10%) and blood (10%) are contained within a rigid and constant volume compartment (the skull). Any volume change involving one of these components will be compensated by adaptive changes in the volume of the remaining components. When the compensatory mechanisms are exhausted, intracranial hypertension (ICH) ensues and is characterized by increased intracranial pressure (ICP) above 20 mmHg. Acute ICH may be caused by head trauma associated with hematomas, stroke, cerebral aneurysm, subarachnoid hemorrhage (SAH) and other causes.(1)

Increased ICP may cause changes in gastrointestinal motility as well as water and electrolyte absorption. Studies have evaluated different means of food administration to brain injury patients as tool to reduce gastrointestinal symptoms. Of note, food intolerance may be associated with increased morbidity and increased hospital stay costs.(2,3)

Considering the paucity of both national and international studies correlating SAH, ICH and gastric emptying (GE), the main objective of this paper is to compare and discuss physiological and pathophysiological related to SAH, ICH and gut motility.



A literature search was conducted to analyze the pattern of gut motility following acute brain injury with ICH. Articles discussing possible therapeutic approaches for ICH-related gut complications were also evaluated. The literature search included national and international health sciences journals, and we searched for articles related to the brain-gastrointestinal tract functional axis and its behavior either in experimental animal models of brain injury or acute brain injury patients. Using the inclusion criteria, a web based search was conducted on the following electronic libraries: Scientific Electronic Library Online (Scielo)©, Periódicos/Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)©, PubMed/Medline© and Google Scholar Beta©.

Twenty-five articles published between 1982 and 2010 were selected. Of those, eleven focused on the influence of ICH on gut motility (GM), ten discussed means of nutrition of administration in moderate to severe head trauma (HT) (Glasgow coma scale < 8), and finally, four articles discussed the main metabolic changes in head trauma subjects, with an emphasis on nutritional support.

Influence of intracranial hypertension on gut motility

Eleven articles about ICH influence about gut motility were analyzed. Five (45.4%) were related to gastric and intestinal emptying, four (36.3%) focused on pressure changes throughout the gastrointestinal tract (GIT) (two studied the amplitude and frequency of food propellant contractions, and the other two analyzed the inferior esophageal sphincter behavior under ICH conditions), and two (18.1%) studies evaluated GIT electrical activity, studying the migratory myoelectric complex by means of body surface electrodes or electrogastrogram. Of all of the articles, two (18.8%) reported that HIC variation is directly proportional to gastric contraction intensity, based on a GE analysis of the amplitude and frequency of contractions in anesthetized rats with intra-cerebral cannulation-induced ICH. The remaining nine (81.8%) articles found that increased ICP is related to slower GIT transit, and this food bolus transit delay is associated with intolerance to enteral nutrition. Pharmacological intervention to accelerate the GIT was evaluated in one of the analyzed articles. Another study was designed to evaluate the association between ICP changes in thirty-seven intracranial tumor patients who performed Valsalva's maneuver during evacuation. All patients performed the maneuver, independent of constipation, and no increased ICP decompensation was observed. Additional studies details are displayed on chart 1.

Forms of nutrition and means of administration in moderate to severe HT patients

Ten studies analyzing the best forms of nutrition for HT patients were evaluated. Five (50%) assessed the best ways to deliver nutrition to these patients, two (20%) analyzed nutrition progression in the days following the HT, two (20%) evaluated the benefits of enteral versus parenteral nutrition, and one (10%) discussed tolerance of enteral nutrition. Regarding the means of administration, nasogastric (NG) and nasojejunal (NJ) tubes were compared. One of the articles concluded that the best caloric supply, nitrogen balance and nitrogen consumption were achieved with an NJ tube, and this was also associated with less infections and shorter lengths of stay. Another article concluded that patients develop moderate food intolerance when fed proximal to the ligament of Treitz, as shown by a better tolerance achieved by the group of patients fed distal to this ligament. Endoscopic percutaneous feeding, evaluated by one article, showed good nutritional support. Continuously administered food was better tolerated than bolus administration. Two of the analyzed studies agreed that prokinetic agents are ineffective for patients receiving enteral nutrition.

Regarding nutrition progression, six months was established by one of the articles as the time when the patient returns to normal eating habits, but most patients in this study showed signs of malnutrition. Early nutrition support was related to lower mortality rates.

Parenteral nutrition was shown to be more beneficial than enteral nutrition for post-HT patients, as it did not interfere with either conventional ICH control therapy or incremental ICP in most of the patients. Another comparative trial reported a 44.4% death rate among patients receiving enteral nutrition, compared with no deaths among those receiving parenteral nutrition during the hospital rehabilitation phase. Enteral nutrition tolerance was inversely proportional to ICP and injury severity. Chart 2 summarizes the ten evaluated articles.

Metabolic changes in head injury subjects

All of the four analyzed articles (100%) considered appropriate nutrition fundamental for meeting post-trauma ICH hypermetabolism requirements, for better clinical outcomes and for reducing the morbidity and mortality of patients. Independent of the food intolerance developed by most of enteral nutrition patients, there was a consensus among all articles that failing to supply metabolic requirements is an important predictor of mortality. However, in one of the articles, excessive caloric support during the first days after a brain injury was associated with additional stress.



SAH is an example of an injury that causes an increase in ICP, resulting in high morbidity levels. It is caused mainly by traumatic brain injuries and is seen in up to 59% of severe HT cases. SAH is a poor prognosis indicator in HT patients, especially when the Glasgow coma scale rating is less than or equal to thirteen. Ideal treatment of these patients is based on intensive neurological measures. GIT changes in patients with altered consciousness levels may involve emesis and aspiration of gastric contents to the trachea and bronchial tree, with increased morbidity.(4-8) Acute gastric dilation and delayed GE are relevant pathophysiological changes in ICH patients, and normalization of these disturbances is useful for effective clinical management. However, the mechanisms of gastrointestinal changes in human ICH patients are still poorly understood.(9-12)

GE is modulated by ANS action. Gut motility disorders in HT patients may be directly caused by the trauma mechanics or may be due to neural injury or changes in the release of mediators. ICH leads to a biphasic systemic autonomous stimulation. It results from hyperactivity of the parasympathetic and sympathetic systems at different times.(13) Recent experimental trials have shown secondary abnormal autonomic responses in patients with increased ICP, with fast GE during the initial phase and delayed gastric transit in a later phase.(13)

The parasympathetic system is known to modulate GIT activity, regulating both its motility and hydroelectrolytic dynamics. During deglutition, the proximal region of the stomach relaxes in conjunction with the inferior esophageal sphincter.(14) Intraluminal pressure drops in both regions before the food bolus arrives due to smooth muscle relaxation in these regions. Next, stomach pressures gradually return to previous levels. Therefore, large volumes of food may be ingested and stay in the stomach with minimal intra-gastric pressure increase. For instance, the human stomach is able to receive 1,600 mL of air with a 10 mmHg pressure increase.(15) Receptive relaxation is mediated by a neural reflex involving both afferent and efferent vagus nerve pathways. When this nerve is transected, receptive relaxation is abolished, the stomach becomes less distensible, and the gastric contractility increase seen with increased ICP is blocked.(16)

ANS modulation and pharmacological basis for GIT autonomic dysregulation therapy

Based on the physiology of ANS and GIT interactions, several pharmacological trials were conducted to establish the actual pathophysiological role of the ANS on GIT changes following brain injury with ICH. Cisapride is an effective prokinetic agent that has been clinically approved for use in reflux esophagitis, gastroparesis and dyspepsia. Cisapride is believed to work by increasing cholinergic activity mediated by 5-HT4 receptors. Cisapride can partially revert ICH-induced inhibition of GE.(17,19) Carbachol, a muscarinic acetylcholine receptor inhibitor, reverted the ICP increase-induced GE inhibition. However, this study reported better protection with lower carbachol doses, which was a peculiar finding. It is likely that the augmented autonomic ganglia nicotinic activity induced by higher carbachol doses could partially suppress the gastric prokinetic effects of the drug.(20)

Data on sympathetic and parasympathetic activity modulation indicate that changes in the activity of these systems may play an important pathophysiologic role in ICH-induced GE inhibition. Support of cholinergic activity may be useful to normalize this inhibitory effect.(20) Sympathetic nerves have adrenergic efferent fibers to the stomach, which inhibit gastric motility and are mediated by α-adrenergic pre-synaptic receptors present in intramural cholinergic neurons.(21,22) Alpha-adrenergic receptors were found centrally in the triggering chemoreceptor zone, and blockade of these receptors appears to prevent noradrenalininduced emesis.(23) Increased ICP leads to activation of medullary centers, primarily by pressure transmission to the brain troncus or secondarily by hypothalamic activation of descending modulatory pathways. Active descending discharge in turn leads to a systemic hyper-adrenergic response, including the splanchnic sympathetic pathway.(24) How this sympathetic activation is able to act on gastric motility and gastric complacency (GC) is still under discussion and requires additional studies. Animals that underwent splanchnicectomy and celiac gangliectomy had no changes in gastric volume (GV) upon ICP increase, suggesting that the ICP-induced stomach tonus increase phenomenon is mediated by a splanchnic pathway.(25)

Prazosin, a type α1 adrenergic inhibitor, reduces vomiting after ICP increase. This was seen following both peripheral and central dosing of the drug, although the best effects were seen with intra-ventricular brain administration.(26) Since then, many emesis-causing stimuli have been shown to delay GE. Therefore, the effects of prazosin on ICP-induced GE inhibition were investigated, given its effectiveness against vomiting induced by the same stimuli. However, both centrally and peripherally administered prazosin failed to improve ICH-induced GE inhibition.(26) In contrast, specific noradrenergic blocking drugs lead to a partial reversion of ICP-induced GE inhibition. Prazosin was ineffective in increasing GE, suggesting that increased sympathetic activity may be responsible for GE inhibition.(26)

Clonidine, an α2-adrenergic agonist, inhibits gastrointestinal transit following both central and peripheral administration, and this effect is mediated by the vagus. However, it failed to affect ICP-induced GE inhibition, either because the ICP-induced sympathetic discharge was insufficient or because the clonidine effect, mediated by the vagus nerve, was antagonized.(27,28)



These GIT changes in severe brain injury patients led us to discuss the use of artificial nutrition for patients with increased ICP. The hypermetabolism and hyper-catabolism of these patients require higher nutritional supplies.(29) Infection is common and prolongs the recovery time.(30) Therefore, appropriate nutrition support may reduce susceptibility to sepsis and increase immunocompetence.(2,31) Acute gastric dilation and delayed GE may be pathophysiologically relevant for HT patients. Normalization of these factors may be useful for central nervous system (CNS) injury patients.(9)

An important article evaluated the nutrition of patients with severe HT and analyzed the time of beginning enteral nutrition and the calories supplied. The probability of survival increased when enteral nutrition was started earlier and with higher caloric supplies. Mortality was two-and four-fold higher among patients for whom enteral nutrition was not started within the first 5 and 7 days after HT, respectively. It should be highlighted that a minimum of 25 kcal/kg/day was associated with improved prognosis.(3)

Early nutrition support via parenteral nutrition is more effective than enteral nutrition for supplying energy, proteins and fluids after neurological injury. (32-34) However, enteral nutrition has been reported to be more beneficial than parenteral nutrition, given its lower cost, lower infection risk, protection of intestinal epithelium integrity, improvement of immunocompetence and attenuation of the metabolic stress response during the illness critical phase.(35) Some severe HT patients, however, cannot tolerate enteral nutrition and show increased gastric residues, prolonged paralytic ileus, abdominal distension and diarrhea.(35) In this clinical condition, enteral nutrition success appears to be inversely correlated with the ICP and trauma severity. The mechanism of this relationship may be multi-factorial. Hypoalbuminemia is another cause of unsuccessful enteral nutrition found in HT patients. In this condition, enteral absorption ability is impaired, as albumin is responsible for maintaining GIT oncotic pressure.(36)

Increases in ICP as a result of SAH induce massive increases in sympathetic activity, which is responsible for several peripheral symptoms as a response to changes in the brain.(11) This emphasizes the pathophysiological influence of sympathetic stimulation via its gastric motility inhibitory effect and the ability of ICH to change gastrointestinal dynamics, including its motility and hydroelectrolytic absorption. It should be emphasized that these GIT changes may be essential for homeostatic stabilization in conditions of hemodynamic instability. Volume restitution and immediate survival upon bleeding in monogastric animals, such as rats and rabbits, are impaired in previously enterectomized or fasting animals.(36) Observations of model animals are key to understanding the difficulties in managing nutrition and blood volume in intensive care patients progressing with secondary ICH following severe HT.(36)



ICH is a complex SNC injury phenomenon that has two different phases, which are influenced by autonomous stimulation. Most of the contemporary trials analyzed in this review support the double SNC stimulation theory.

Early enteral nutrition in patients with severe HT is important for managing the care of polytrauma patients. However, achieving adequate energy supply in this way may be challenging in neurological injury patients, since delayed GE is a common clinical contraindication for enteral feeding. In these cases, parenteral nutrition should be considered. Therefore, the ICP level at which a hypercatabolic patient can be safely fed via enteral nutrition should be established because this method supports GIT transit, nutrient absorption and more effective recovery.



1. Guyton AC, Hall JE. Regulação renal de potássio, cálcio, fosfato e magnésio; Integração dos mecanismos renais para o controle o volume sanguíneo e do volume do líquido extracelular. In: Guyton AC, Hall JE. Tratado de fisiologia médica. 11a ed. Rio de Janeiro: Guanabara Koogan; 2006.p.365-81.

2. Rapp RP, Young B, Twyman D, Bivins BA, Haack D, Tibbs PA, Bean JR. The favorable effect of early parenteral feeding on survival in head-injury patients. J Neurosurg. 1983;58(6):906-12.

3. Härtl R, Gerber LM, Ni Q, Ghajar J. Effect of early nutrition on deaths due to severe traumatic brain injury. J Neurosurg. 2008;109(1):50-6.

4. Rhoney DH, Parker DJ Jr, Formea CM, Yap C, Coplin WM. Tolerability of bolus versus continuous gastric feeding in brain-injured patients. Neurol Res. 2002;24(6):613-20.

5. Kirshtein B, Hilzenrat N, Yaari A, Souter KJ, Artru AA, Shapira Y, Sikuler E. Hemodynamic changes in visceral organs following closed head trauma in rats. Resuscitation. 2008;77(1):127-31.

6. Torres AC, Diccini S. Constipação intestinal em pacientes com tumores intracranianos. Rev Latinoam Enferm. 2006;14(3):397-404.

7. Thor PJ, Gościński I, Kolasińska-Kloch W, Madroszkiewicz D, Madroszkiewicz E, Furgała A. Gastric myoelectric activity in patients with closed head brain injury. Med Sci Monit. 2003;9(9):CR392-5.

8. Matthews DE, Heimansohn DA, Papaila JG, Lopez R, Vane DW, Grosfeld JL. The effect of increased intracranial pressure (ICP) on gastric motility. J Surg Res. 1988;45(1):60-5.

9. Collins WF, Venes JL, Wagner FC, Spencer DD. Neurologic surgery. In: Schwartz SI, editor. Principles of surgery. New York: McGraw-Hill; 1979. p.1759-807.

10. Garrick T, Mulvihill S, Buack S, Maeda-Hagiwara M, Tache Y. Intracerebroventricular pressure inhibits gastric antral and duodenal contractility but not acid secretion in conscious rabbits. Gastroenterology. 1988;95(1):26-31.

11. Schnoor J, Zoremba N, Korinth MC, Kochs B, Silny J, Rossaint R. Short-term elevation of intracranial pressure does neither influence duodenal motility nor frequency of bolus transport events: a porcine model. BMC Emerg Med. 2006;6:1.

12. Mulvihill SJ, Pappas TN, Debas HT. Effect of increased intracranial pressure on gastric acid secretion. Am J Surg. 1986;151(1):110-6.

13. Ott L, Young B, Phillips R, McClain C, Adams L, Dempsey R, et al. Altered gastric emptying in the head injured patient: relationship to feeding intolerance. J Neurosurg. 1991;74(5):738-42.

14. Kelly KA. Gastric emptying of liquids and solids: roles of proximal and distal stomach. Am J Physiol. 1980;239(2):G71-6. Review.

15. Kumar D, Wingate D. An illustrated guide to gastrointestinal motility. 2nd ed. New York: Churchill Livingstone; 1993.

16. Oliveira RB, Ceneviva R, Troncon LE. Lack of correlation between intragastric pressure and early gastric emptying rate after proximal gastric vagotomy. Braz J Med Biol Res. 1985;18(4):471-5.

17. Tonini M, Rizzi CA, Manzo L, Onori L. Novel enteric 5-HT4 receptors and gastrointestinal prokinetic action. Pharmacol Res. 1991;24(1):5-14. Review.

18. Onat F, Yegen B, Berkman K, Oktay S. The hypotensive effect of cisapride in rat. Gen Pharmacol. 1994;25(6):1253-6.

19. Bockaert J, Fozard JR, Dumuis A, Clarke DE. The 5-HT4 receptor: a place in the sun. Trends Pharmacol Sci. 1994;13(4):141-5.

20. Kacker V, Mehta VS, Gupta YK. Acute intracranial hypertension-induced inhibition of gastric emptying: evaluation in conscious rats. Eur J Pharmacol. 1999;369(1):65-72.

21. Abrahamsson H, Glise H. Sympathetic nervous control of gastric motility and interaction with vagal activity. Scand J Gastroenterol Suppl. 1984;89:83-7.

22. Gillespie JS, Khoyi MA. The site and receptors responsible for the inhibition by sympathetic nerves of intestinal smooth muscle and its parasympathetic motor nerves. J Physiol. 1977;267(3):767-89.

23. Jenkins LC, Lahay D. Central mechanisms of vomiting related to catecholamine response: anaesthetic implication. Can Anaesth Soc J. 1971;18(4):434-41.

24. Marmarou A. The pathophysiology of brain edema and elevated intracranial pressure. Cleve Clin J Med. 2004;71 Suppl 1:S6-8. Review.

25. Cristino Filho G. Efeito da hipertensão intracraniana sobre a complacência gástrica de ratos anestesiados: caracterização do fenômeno e dos mecanismos neurais. [tese]. Ceará: Faculdade de Medicina da Universidade Federal do Ceará; 2004. 148 f.

26. Kacker V, Gupta YK. An experimental model to study intracranial hypertension-induced vomiting in conscious dogs. Methods Find Exp Clin Pharmacol. 1996;18(5):315-20.

27. Payen D, Quintin L, Plaisance P, Chiron B, Lhoste F. Head injury: clonidine decreases plasma catecholamines. Crit Care Med. 1990;18(4):392-5.

28. Tadano T, Kisara K, Stewart JJ. A comparison of peripheral and central effects of clonidine on rat intestinal transit. Res Commun Chem Pathol Pharmacol. 1992;78(2):161-79.

29. McClain CJ, Twyman DL, Ott LG, Rapp RP, Tibbs PA, Norton JA, et al. Serum and urine zinc response in headinjured patients. J Neurosurg. 1986;64(2):224-30.

30. Antonacci AC. Immune dysfunction and immunomodulation following trauma. In: Gallin JI, Fauci AS, editors. Advances in host defense mechanisms. New York: Raven Press; 1986. p.81-104.

31. Young B, Ott L, Twyman D, Norton J, Rapp R, Tibbs P, et al. The effect of nutritional support on outcome from severe head injury. J. Neurosurg. 1987;67(5):668-76.

32. Berger R, Adams L. Nutritional support in the critical care setting (Part 1). Chest. 1989;96(1):139-50. Review.

33. Berger R, Adams L. Nutritional support in the critical care setting (Part 2). Chest. 1989;96(2):372-80.

34. Christman JW, McCain RW. A sensible approach to the nutritional support of mechanically ventilated critcally ill patients. Intensive Care Med. 1993;19(3):129-36.

35. Norton JA, Ott LG, McClain C, Adams L, Depmsey RJ, Haack D, et al. Intolerance to enteral feeding in the braininjured patient. J Neurosurg. 1988;68(1):62-6.

36. Bettice D. The cause of vomiting of tube feedings by neurosurgical patients. J Neurosurg Nurs. 1971;3(2):93-112.

37. Livingston EH, Passaro EP Jr, Garrick T. Elevated intracranial pressure stimulates gastric contractility in the rat. J Surg Res. 1991;50(2):106-10.

38. Kao CH, ChangLai SP, Chieng PU, Yen TC. Gastric emptying in head-injured patients. Am J Gastroenterol. 1998;93(7):1108-12.

39. Shteyer E, Rothman E, Constantini S, Granot E. Gastroesophageal reflux in infants with hydrocephalus before and after ventriculo-peritoneal shunt operation. Pediatr Neurosurg. 1998;29(3):138-41.

40. Vane DW, Shiffler M, Grosfeld JL, Hall P, Angelides A, Weber TR, Fitzgerald JF. Reduced lower esophageal sphincter (LES) pressure after acute and chronic brain injury. J Pediatr Surg. 1982;17(6):960-4.

41. Cristino-Filho G, Leal PR, Lira GH, Souza SG, Rola FH, Oliveira RB, Santos AA. Acute intracranial hypertension increases gastri tonus in anesthetized rats. Autonomic Neuroscience: Basic & Clinical. 2009;146(1-2):95-101.

42. Klodell CT, Carroll M, Carrillo EH, Spain DA. Routine intragastric feeding following traumatic brain injury is safe and well tolerated. Am J Surg. 2000;179(3):168-71.

43. Graham TW, Zadrozny DB, Harrington T. The benefits of early jejunal hyperalimentation in the head-injured patient. Neurosurgery 1989;25(5):729-35.

44. Krakau K, Hansson A, Karlsson T, de Boussard CN, Tengvar C, Borg J. Nutritional treatment of patients with severe traumatic brain injury during the first six months after injury. Nutrition. 2007;23(4):308-17.

45. Kozar RA, McQuiggan MM, Moore EE, Kudsk KA, Jurkovich GJ, Moore FA. Postinjury enteral tolerance is reliably achieved by a standardized protocol. J Surg Res. 2002;104(1):70-5.

46. Bochicchio GV, Bochicchio K, Nehman S, Casey C, Andrews P, Scalea TM. Tolerance and efficacy of enteral nutrition in traumatic brain-injured patients induced into barbiturate coma. JPEN J Parenter Enteral Nutr. 2006;30(6):503-6.



Submission On-line

Indexed in




Associação de Medicina Intensiva Brasileira - AMIB

Rua Arminda nº 93 - 7º andar - Vila Olímpia - São Paulo, SP, Brasil - Tel./Fax: (55 11) 5089-2642 | e-mail: [email protected]

Cookie Policy

GN1 - Systems and Publications