Comité NeuroAnestesiaSCA

1. FLUIDO-TERAPIA EN
NEUROCIRUGÍA
CASO CLÍNICO
Gerupo Neuroanestesia FSFB

2. Identificación
• RJOA
• Masculino
• 23 años
• Natural de Arauca
• Procedente de Bogota
• Estudiante de Medicina
• Soltero
• Pago Directo
• 27/07/17

3. Motivo de Consulta
• Cefalea, síntomas visuales y lesión intraventricular.

4. Enfermedad actual
• Paciente quien consulta por cuadro clínico de
aproximadamente 3 meses de evolución, consistente en
episodios de cefalea biparietal tipo presión que en
ocasiones lo han despertado, asociado a fosfenos y tinitus
en forma intermitente. Refiere que en el último mes ha
presentado problemas con la expresión verbal y la
organización sintáctica del lenguaje, visión borrosa, por lo
que fue estudiado documentándose lesión localizada en el
atrio ventricular cerebral izquierdo. Ingresa para manejo
quirúrgico.

5. Antecedentes
• Patologicos: Hipotiroidismo subclinico
• Farmacologicos: Dexametasona, Acetaminofen,
Omeprazol.
• Quirúrgicos: Niega
• Anestésicos: Niega
• Alérgicos: Niega
• Tóxicos: Niega
• Transfusionales: Niega

6. Examen físico
• Buen estado general, afebril, sin signos de dificultad respiratoria ni
respuesta inflamatoria sistémica.
• TA: 129/78 FC: 82 FR: 18 SaO2: 98% T: 36ºC
EVA: 0 Peso : 74 Talla : 172 IMC: 25.01
• Neurológico: alerta, consciente, orientado en persona, tiempo y
lugar. Resto de funciones mentales superiores conservadas. Pares
craneanos con isocoria de 3mm normorreactivas, campimetría por
confrontación normal. Agudeza visual 20/20 sin corrección.
Sensibilidad y simetría facial cosnervadas. Resto de pares bajos sin
alteraciones. Motor con fuerza 5/5 en 4 extremidades, reflejos ++/
++++ simétricos, respuesta plantar flexora bilateral. Sensibilidad
conservada. No dismetría ni disdiadococinesia. Nistagmo
optoquinético conservado. No signos meníngeos.

7. Paraclínicos
• PTT 29.8/29.6 PT 12.9/11.1 INR: 1.16
• LEUCOS 15700 HB 15.6 HTO: 47 PLAQ: 371700
• GLIC: 88 CRSR: 0.66 BUN 17

8. Imágenes
• TAC y resonancia magnética contrastada muestran
lesión intraventricular en atrio izquierdo, probable
meningioma, que produce importante edema
vasogénico y dilatación ipsilateral de los cuernos
tempora y occipital del ventrículo lateral.

15. Diagnósticos
• Hipotiroidismo Subclinico
• Meningioma intraventricular dependiente del atrio
izquierdo

16. Intraoperatorio
• Monitoreo: saturación de oxígeno, tensión arterial, visoscopio, lineas
invasivas (arterial y pvc), monitoria de la relajacion (tren de cuatro), de la
profundidad anestesica con electroencefalograma procesado (bis),
capnografia y termometro esofagico.
• Inducción anestesica con propofol (TCI) remifentanil (TCI) y lidocaina
(mg/kg/hora)
• Relajación muscular con rocuronio
• Videolaringoscopia grado I/IV con C-MAC. Tubo flexoanillado número 8.
• Mantenimiento anestésico con propodol (TCI), remifentanil (TCI),
dexmedetomidina (mcg/kg/hora), lidocaina (mg/kg/hora).
• Linea arterial, CVC YEI, bloqueo cuero izquierdo y cervicar superficial.
• Profilaxis antiemetica: dexametasona, ondansetron, omeprazol.

19. • GASES VENOSOS
• 10:58 SAT 84,2% HB 15,4 LAC 2,2 HTO 47,2
• GASES ARTERIALES
• 11:20 PH 7,4 PCO2 35,1 PO2 220 HCO3 22,8 BE
-1,6 GLU 111 LAC 2,2 HB 15,4 HTO 47,2 CA 1,1
CL 106 K 3,7 NA 139
Intraoperatorio

21. • GASES VENOSOS
• 12:07 SAT 82,2% HB 14,7 LAC 2,1 HTO 44,9
• GASES ARTERIALES
• 12:05 PH 7,4 PCO2 34,6 PO2 242 HCO3 21,5 BE
-2,8 GLU 116 LAC 2,2 HB 15,2 HTO 46,5 CA 1,1
CL 109 K 3,5 NA 141
Intraoperatorio

23. • GASES ARTERIALES
• 14:05 PH 7,34 PCO2 40,2 PO2 224 HCO3 21,7 BE
-3,8 GLU 129 LAC 2,3 HB 13,4 HTO 41,1 CA 1,1
CL 111 K 4,3 NA 144
Intraoperatorio

25. • GASES ARTERIALES
• 15:00 PH 7,34 PCO2 39,1 PO2 174 HCO3 21,4 BE -4,0
GLU 127 LAC 2,3 HB 12,9 HTO 39,7 CA 1,1 CL 112 K
4 NA 147
• MANITOL 20%: 185 CC.
• DIURESIS: 3400
• SANGRADO: 400
• LIQUIDOS: 300 ML ALBUMINA, 2600 ML DE SSN.
Intraoperatorio

26. Intraoperatorio
• Finaliza procedimiento quirúrgico.
• Analgesia multimodal con infucion intraoperatoria de
dexmedetomidina y lidocaina, mas acetaminofen.
• Se extuba paciente sin complicaciones y se traslada a
unidad de cuidados intensivos.
• Signos vitales: frecuencia cardíaca 72/minuto, tensión
arterial 146/82 , saturación 99%, frecuencia
respiratoria 18/minuto

27. Post-Operatorio
• Resonancia magnética de control sin evidencia de
lesión residual, cambios postquirúrgicos.
• Paciente con excelente evolución postoperatoria, sin
déficit neurológico posterior a intervención,
hemodinámicamente estable. Se decide egreso. Se dan
recomendaciones y signos de alarma, los cuales
comprende y acepta.

28. Que conoce del uso de Albumina
en pacientes Neuroquirúrgicos?

29. Subgrupo Trauma: Beneficio SSN
0.9% sobre albúmina
RR muerte > Pacientes con lesión
cerebral asociada
Finfer S, Bellomo R, Boyce N, French J, Myburgh J, Norton R: A comparison of albumin and saline for fluid resuscitation in the intensive care unit. N Engl J Med 2004, 350:2247–2256.
No diferencias en mortalidad
Análisis subgrupos: Tendencia <
Mortalidad en Sepsis con Albúmina
Ensayo multicéntrico
SSN 0.9% Vs Albúmina
6.997 Pacientes
(Saline versus Albumin Fluid Evaluation)

30. original article
The new engl and jour nal o f medicine
Saline or Albumin for Fluid Resuscitation
in Patients with Traumatic Brain Injury
The SAFE Study Investigators*
The Saline versus Albumin Fluid Evalua-
tion (SAFE) study is a collaboration of the
Australian and New Zealand Intensive Care
Society Clinical Trials Group, the Austra-
lian Red Cross Blood Service, and the
George Institute for International Health.
The writing committee of the SAFE–Trau-
matic Brain Injury study (John Myburgh,
M.D., Ph.D., D. James Cooper, M.D., Si-
mon Finfer, M.D., Rinaldo Bellomo, M.D.,
Robyn Norton, Ph.D., M.P.H., Nicole Bish-
op, B.Sc., Sing Kai Lo, Ph.D., and Shirley
Vallance, R.N.) takes responsibility for
the content and integrity of this article.
Address reprint requests to Dr. Myburgh
at ANZICS Clinical Trials Group, Level 3,
10 Ievers Terrace, Carlton, VIC 3053, Aus-
tralia, or at j.myburgh@unsw.edu.au.
*The Saline versus Albumin Fluid Evalua-
tion (SAFE) study investigators are listed
in the Appendix.
N Engl J Med 2007;357:874-84.
Copyright © 2007 Massachusetts Medical Society.
Abstr act
Background
The Saline versus Albumin Fluid Evaluation study suggested that patients with trau-
matic brain injury resuscitated with albumin had a higher mortality rate than
those resuscitated with saline. We conducted a post hoc follow-up study of patients
with traumatic brain injury who were enrolled in the study.
Methods
For patients with traumatic brain injury (i.e., a history of trauma, evidence of head
trauma on a computed tomographic [CT] scan, and a score of ≤13 on the Glasgow
Coma Scale [GCS]), we recorded baseline characteristics from case-report forms, clini-
cal records, and CT scans and determined vital status and functional neurologic out-
comes 24 months after randomization.
Results
We followed 460 patients, of whom 231 (50.2%) received albumin and 229 (49.8%)
received saline. The subgroup of patients with GCS scores of 3 to 8 were classified
as having severe brain injury (160 [69.3%] in the albumin group and 158 [69.0%] in
the saline group). Demographic characteristics and indexes of severity of brain in-
jury were similar at baseline. At 24 months, 71 of 214 patients in the albumin group
(33.2%) had died, as compared with 42 of 206 in the saline group (20.4%) (relative risk,
1.63; 95% confidence interval [CI], 1.17 to 2.26; P=0.003). Among patients with se-
vere brain injury, 61 of 146 patients in the albumin group (41.8%) died, as compared
with 32 of 144 in the saline group (22.2%) (relative risk, 1.88; 95% CI, 1.31 to 2.70;
P<0.001); among patients with GCS scores of 9 to 12, death occurred in 8 of 50 pa-
tients in the albumin group (16.0%) and 8 of 37 in the saline group (21.6%) (relative
risk, 0.74; 95% CI, 0.31 to 1.79; P=0.50).
Conclusions
In this post hoc study of critically ill patients with traumatic brain injury, fluid resus-
citation with albumin was associated with higher mortality rates than was resusci-
tation with saline. (Current Controlled Trials number, ISRCTN76588266.)
The new engl and jour nal of medicine
Our study provides post hoc data to guide the
choice of resuscitation fluid in patients with trau-
matic brain injury, but the biologic mechanisms
for the observed differences in mortality are un-
clear. Because there was no difference in hemody-
namic-resuscitation end points or in the cause and
time of death between the two groups, one mech-
anism may be exacerbation of vasogenic or cyto-
toxic cerebral edema induced by the administra-
tion of albumin.35,36 Initial intracranial pressure
tended to be higher in the albumin group, al-
though this difference was not substantial. The
magnitude of the increase in intracranial pressure
may also have been masked by therapeutic inter-
ventions, some of which may have had adverse
effects. Furthermore, we defined post-randomiza-
tion intracranial hypertension as an intracranial
pressure that exceeded 30 mm Hg for two con-
secutive readings at least 30 minutes apart, and it
remains possible that differences in lesser degrees
of intracranial hypertension may have occurred
and could explain the difference in outcome we
observed. Further detailed analyses of biologic
mechanisms associated with intracranial hyper-
tension are required.
In conclusion, in our study comparing albumin
with saline for intravascular fluid resuscitation in
the ICU, higher mortality rates were observed
among patients with severe traumatic brain injury
who received 4% albumin than among those who
received saline. These findings suggest that sa-
line is preferable to albumin during the acute re-
100
80
90
70
60
50
0
100
80
90
70
60
50
0
0 4 8 12 16 2420 28
Albumin
Saline
P=0.007
0 100 200 300 400 600500 700
Albumin
Saline
P=0.007
AUTHOR:
FIGURE:
RETAKE
ICM
CASE Revised
REG F
1st
2nd
3rd
Myburgh
2 of 2
Figure 2. Kaplan–Meier Estimates of the Probability
of Survival.
The figure shows the probability of survival at 28 days
(Panel A) and at 24 months (Panel B) among patients
Saline or Albumin in Patients with Traumatic Brain Injury
Table 3. Primary and Secondary Outcomes.*
Outcome Albumin Group Saline Group Relative Risk (95% CI) P Value
All patients
Deaths — no./total no. (%)
Within 28 days 61/231 (26.4) 36/229 (15.7) 1.68 (1.16–2.43) 0.005
Within 6 mo 68/221 (30.8) 40/217 (18.4) 1.67 (1.18–2.35) 0.003
Within 12 mo 69/220 (31.4) 40/216 (18.5) 1.69 (1.20–2.38) 0.002
Within 24 mo 71/214 (33.2) 42/206 (20.4) 1.63 (1.17–2.26) 0.003
Favorable score on the GOSe at 24 mo 96/203 (47.3) 120/198 (60.6) 0.78 (0.65–0.94) 0.007
Survivors at 24 mo 96/132 (72.7) 120/156 (76.9) 0.95 (0.83–1.08) 0.41
Patients with a GCS score of 3–8
Deaths — no./total no. (%)
Within 28 days 55/160 (34.4) 30/158 (18.9) 1.83 (1.23–2.71) 0.002
Within 6 mo 60/154 (38.9) 32/149 (21.5) 1.81 (1.26–2.61) 0.001
Within 12 mo 61/153 (39.9) 32/149 (21.5) 1.86 (1.29–2.67) 0.001
Within 24 mo 61/146 (41.8) 32/144 (22.2) 1.88 (1.31–2.70) <0.001
Favorable score on the GOSe at 24 mo 51/139 (36.7) 77/140 (55.0) 0.67 (0.51–0.87) 0.002
Survivors at 24 mo 51/78 (65.4) 77/108 (71.3) 0.92 (0.75–1.12) 0.39
Patients with a GCS score of 9–12
Deaths — no./total no. (%)
Within 28 days 6/53 (11.3) 5/44 (11.4) 0.99 (0.33–3.05) 0.99
Within 6 mo 6/49 (12.2) 6/41 (14.6) 0.84 (0.29–2.40) 0.74
Within 12 mo 6/49 (12.2) 6/40 (15) 0.82 (0.29–2.34) 0.71
Within 24 mo 8/50 (16.0) 8/37 (21.6) 0.74 (0.31–1.79) 0.50
Favorable score on the GOSe at 24 mo 36/49 (73.5) 24/36 (66.7) 1.10 (0.83–1.47) 0.51
Survivors at 24 mo 36/44 (81.8) 24/33 (72.7) 1.13 (0.88–1.43) 0.34
* GCS denotes Glasgow Coma Scale, and GOSe denotes Extended Glasgow Outcome Scale, on which 8 indicates mini-
mal or no disability and 1 indicates death. Scores of 5 to 8 on the GOSe are considered favorable.

31. Review article
Clinical indications for the albumin use: Still a controversial issue
Paolo Caraceni ⁎, Marco Domenicali, Alessandra Tovoli, Lucia Napoli, Carmen Serena Ricci,
Manuel Tufoni, Mauro Bernardi
U.O. Semeiotica Medica, Department of Medical and Surgical Sciences, Alma Mater Studiorum, University of Bologna, Bologna, Italy
a b s t r a c ta r t i c l e i n f o
Article history:
Received 13 May 2013
Received in revised form 21 May 2013
Accepted 24 May 2013
Available online xxxx
Keywords:
Albumin
Liver cirrhosis
Ascites
Fluid resuscitation
Sepsis
Human serum albumin (HSA) is the most abundant circulating protein and accounts for about 70% of the
plasma colloid osmotic pressure. Beside the well known capacity to act as plasma-expander, HSA is provid-
ed of many other properties which are unrelated to the regulation of fluid compartmentalization, including
binding and transport of many endogenous and exogenous substances, antioxidant function, immuno-
modulation, anti-inflammatory activity, and endothelial stabilization.
Treatment (hepatorenal syndrome) or prevention (renal failure after spontaneous bacterial peritonitis and post-
paracentesis circulatory dysfunction after large volume paracentesis) of severe clinical complications in patients
with cirrhosis and fluid resuscitation in critically ill patients, when crystalloids and non-proteic colloids are not
effective or contra-indicated, represents the major evidence-based clinical indications for HSA administration.
However, a large proportion of HSA prescription is inappropriate. Despite the existence of solid data against a
real benefit, HSA is still given for nutritional interventions or for correcting hypoalbuminemia per se (without
hypovolemia). Other clinical uses for HSA administration not supported by definitive scientific evidence are
long-term treatment of ascites, nephrotic syndrome, pancreatitis, abdominal surgery, acute distress respira-
tory syndrome, cerebral ischemia, and enteric diseases.
HSA prescription should be not uncritically restricted. Enforcement of clinical practice recommendations has
been shown to allow a more liberal use for indications supported by strong scientific data and to avoid the futile
administration in settings where there is a lack of clinical evidence of efficacy. As a result, a more appropriate HSA
use can be achieved maintaining the health care expenditure under control.
© 2013 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.
1. Introduction
Human serum albumin (HSA) is the most abundant circulating pro-
tein in the body provided of both oncotic and non-oncotic properties.
Administration of exogenous HSA dates back in the World War II when
it was used for fluid resuscitation. Since then, the use of HSA has been ex-
tended to many other diseases since physicians commonly believe in its
efficacy. However, beside some clinical indications supported by solid
scientific evidence, the administration in many other settings is still
under debate or has been disproved by evidence-based medicine. As a
result, clinical practical recommendations have been proposed to ratio-
2. The molecule of albumin
2.1. Structure
HSA is the main circulating protein in healthy individuals (3.5–5 g/dl),
representing about 50% of the total protein content in the plasma. HSA is a
small protein with a molecular weight of 66.5 kDa, consisting of a single
chain of 585 amino acids organized in three repeated homologue
domains (sites I, II, and III), each of which comprised of two separate
sub-domains (A and B). In the human body, HSA assumes a globular
heart-shaped conformation formed by α-helices for about 67%. Of the
Contents lists available at SciVerse ScienceDirect
European Journal of Internal Medicine
journal homepage: www.elsevier.com/locate/ejim
solid data against a real benefit. Other clinical uses for HSA administra-
tion not supported by solid scientific evidence are nephrotic syndrome,
pancreatitis, abdominal surgery, acute distress respiratory syndrome,
cerebral ischemia, and enteric diseases [69–73].
Finally, inappropriate prescription can also occur even in presence of
clinical guidelines and recommendations, i.e. when HSA is prescribed as
first-line treatment for fluid resuscitation even if other cheaper plasma-
expanders are not contraindicated or for chronic treatment of cirrhosis.
5. Impact of clinical recommendations for albumin prescription
Beside the high proportion of inappropriate use, the elevated cost,
the theoretical risk of disease transmission and the existence of more
economical alternatives of comparable efficacy have prompted several
clinical and economical evaluations aiming to rationalize and render
more appropriate the use of HSA [69–73].
ture under control.
Learning points
• Clinical indications for HSA administration have emerged from
evidence-based medicine.
• HSA is the first choice to expand effective volemia in patients with
advanced cirrhosis and should be used to prevent renal failure
after spontaneous bacterial peritonitis and the post-paracentesis
circulatory dysfunction after large volume paracentesis or to diag-
nose and treat hepatorenal syndrome.
• HSA is also the second-line treatment for fluid resuscitation in critical-
ly ill patients when crystalloids and non-proteic colloids are not effec-
tive or contra-indicated. Among the heterogeneous population of ICU
patients, accumulating data indicate that those with sepsis, severe
sepsis, and septic shock benefit more from HSA administration.
Table 2
Practical recommendations for the prescription of human serum albumin at the S. Orsola-Malpighi University Hospital, Bologna, Italy [69].
Acute diseases First-line treatment Second-line treatment
Hypovolemic shock Colloid/crystalloid solutions Human albumin if:
• Sodium intake restriction
• Hypersensitivity to colloid or crystalloids
• Lack of response to combined use of colloids and crystalloid
Major surgery:
• Cardiovascular
• Other surgery
Colloid/crystalloid solutions Human albumin if:
• Lack of response to combined use of colloid/crystalloid
Burns Colloid/crystalloid solutions Human albumin plus crystalloid solutions if:
• Lack of response to colloid or crystalloid solutions alone
• Severe burns (>50% body surface)
Paracentesis Human albumin 8 g/l of removed ascites if paracentesis >4 l
Spontaneous bacterial peritonitis Human albumin 1.5 g/kg at diagnosis and 1 g/kg on third
day + antibiotic therapy
Hepatorenal syndrome Human albumin 1 g/kg at diagnosis followed by
20–40 g/die + vasoconstrictors
Ascites Diuretic treatment Human albumin if:
• Ascites resistant to diuretics
Plasmapheresis Human albumin if plasma changes >20 ml/kg per week
Protein wasting enteropathy/malnutrition Enteral or parenteral nutrition Human albumin if:
• Severe diarrhea (>2 l/die)
• Albuminemia b 2 g/dl
• Clinical hypovolemia
Please cite this article as: Caraceni P, et al, Clinical indications for the albumin use: Still a controversial issue, European Journal of Internal Medicine
(2013), http://dx.doi.org/10.1016/j.ejim.2013.05.015

32. Que conoce del uso de
Soluciones Balanceadas en
pacientes Neuroquirúrgicos?

33. RESEARCH Open Access
Balanced versus chloride-rich solutions for fluid
resuscitation in brain-injured patients: a
randomised double-blind pilot study
Antoine Roquilly1†
, Olivier Loutrel1†
, Raphael Cinotti2
, Elise Rosenczweig3
, Laurent Flet4
, Pierre Joachim Mahe1
,
Romain Dumont1
, Anne Marie Chupin1
, Catherine Peneau1
, Corinne Lejus1
, Yvonnick Blanloeil2
, Christelle Volteau5
and Karim Asehnoune1*
Abstract
Introduction: We sought to investigate whether the use of balanced solutions reduces the incidence of
hyperchloraemic acidosis without increasing the risk for intracranial hypertension in patients with severe brain injury.
Methods: We conducted a single-centre, two-arm, randomised, double-blind, pilot controlled trial in Nantes,
France. Patients with severe traumatic brain injury (Glasgow Coma Scale score ≤8) or subarachnoid haemorrhage
(World Federation of Neurosurgical Society grade III or higher) who were mechanically ventilated were randomised
within the first 12 hours after brain injury to receive either isotonic balanced solutions (crystalloid and hydroxyethyl
starch; balanced group) or isotonic sodium chloride solutions (crystalloid and hydroxyethyl starch; saline group) for
48 hours. The primary endpoint was the occurrence of hyperchloraemic metabolic acidosis within 48 hours.
Results: Forty-two patients were included, of whom one patient in each group was excluded (one consent
withdrawn and one use of forbidden therapy). Nineteen patients (95%) in the saline group and thirteen (65%) in
the balanced group presented with hyperchloraemic acidosis within the first 48 hours (hazard ratio = 0.28, 95%
confidence interval [CI] = 0.11 to 0.70; P = 0.006). In the saline group, pH (P = .004) and strong ion deficit
(P = 0.047) were lower and chloraemia was higher (P = 0.002) than in the balanced group. Intracranial pressure
was not different between the study groups (mean difference 4 mmHg [-1;8]; P = 0.088). Seven patients (35%) in
the saline group and eight (40%) in the balanced group developed intracranial hypertension (P = 0.744). Three
patients (14%) in the saline group and five (25%) in the balanced group died (P = 0.387).
Conclusions: This study provides evidence that balanced solutions reduce the incidence of hyperchloraemic
acidosis in brain-injured patients compared to saline solutions. Even if the study was not powered sufficiently for
this endpoint, intracranial pressure did not appear different between groups.
Trial registration: EudraCT 2008-004153-15 and NCT00847977
The work in this trial was performed at Nantes University Hospital in Nantes, France.
Roquilly et al. Critical Care 2013, 17:R77
http://ccforum.com/content/17/2/R77
Figure 2 Kaplan-Meier curves for hyperchloraemic acidosis. Hyperchloraemic acidosis was defined as the association of hyperchloraemia
(>108 mmol/L) with strong ion difference (SID) (<40 mmol/L). SID = (Na + K + Ca + Mg) - (Cl + lactate). Na; sodium, K; potassium; Ca: calcium;
Mg: magnesium; Cl: chloride.
Roquilly et al. Critical Care 2013, 17:R77
http://ccforum.com/content/17/2/R77
Page 7 of 13
Figure 4 Time course of (A) blood osmolarity, (B) natraemia and (C) intracranial pressure in the saline group and the balanced g
Results are given as medians (IQR). *P < 0.05 versus saline group (significant group effect).
HR: 0.28, [CI] = 0.11 to 0.70; P = 0.006)
MD 4 mmHg [-1;8]; P = 0.088
7(35%) vs 8 (40%) à HTEC (P = 0.744)
3(14%) vs 5 (25%) à Muerte (P = 0.387)

34. Que situaciones especiales de
alteraciones del sodio y el agua
corporal conoce, que puedan
presentarse en pacientes
Neuroquirúrgicos?

35. ↑ AMPc
Canales de
aquaporina 2 en mem
celular
Reabsorción
Luz nefrona
a cel TC
Aquaporina 3-4
Intersticio Renal –
Circulación
> Osm intersticial
Reabsorción úrea del
Luz medular Osmolaridad plasmática regula ADH
Schreckinger M. Diabetes insipidus following resection of pituitary tumors. Clin Neurol Neuros 2013
(115)

36. DI NEFROGÉNICA
• Respuesta inadecuada ADH en túbulos
renales
• Inhabilidad [Orina]
• Medicamentos, hipercalcemia,
enfermedad renal primaria
DI NEUROGÉNICA
• Secreción inadecuada ADH en
hipotálamo
• Hereditaria, idiopática o lesión
• Autoinmune, radiación, trauma,
infección, isquemia, Cx
Schreckinger M. Diabetes insipidus following resection of pituitary tumors. Clin Neurol Neuros 2013 (115)

37. • 24H POP. >80% Células destruidas
• 25% DI transitoria. 0.5%
Permanente
• Poliuria (GU 2mL/Kg/h)
• Orina hipotónica (Gravedad especifica
<1.005)
• Osm U <300 mosm/L. S > 300
mosm/L.
• Hipernatremia (<145mmol/L)
Anesthetic management of patients undergoing pituitary surgery. Acta Clin Croat 2011 (50)209-216
TRATAMIENTO
Desmopresina 0.2 mcg IV-IM
(100-800mcg TID VO)
SS 0.45% o Ingesta agua libre
Monitoreo electrolítico
SÍNTOMAS
Polidipsia/Poliuria
DHT, letargo
Convulsiones

38. • 9-25% Cx trans-esfenoidal
• Manifestaciones 1 sem
• Secreción inadecuada ADH.
Independiente de Osm
• Na <135 mmol/L
• Osm sérica < 280 mmol/L
• Orina concentrada
• Euvolemia
• Función renal normal
Restricción hídrica 800-1000mL/día
SS Hipertónica (Si Na<120mmol/L)
Anesthetic management of patients undergoing pituitary surgery. Acta Clin Croat 2011 (50)209-216
Liberación no controlada ADH por
neuronas hipotalámicas secretoras
de ADH en vías de degeneración,
dañadas en intervención del soma
celular o en sus axones que integran
el tallo hipotálamo-hipofisario

40. Determine las principales
diferencias entre SIHAD y Diabetes
insípida

42. Determine las principales
diferencias entre SIHAD y Cerebro
Perdedor de Sal

44. Resumen