6. You were offered kidneys from 59-year-old male DBD (donor after brain stem death) donor who suffered from SAH (grade 5) complicating cerebral aneurysm. Her baseline S Cr was 60 µmol/L. On admission, S Cr was 75 µmol/L, he also passed 12 L over the last 24 hours.
- Would you accept this donor?
- How do you manage this condition?
the above case is a 59 year old donor who has brain death following cerebral anuerysm rupture….The index donor is an extended criteria donor with history of CVA and also age between 50-60 years…The donor has normal renal functions but the issue seems to be with polyuria….(12L in 24 hours)
I will accept this donor as there is no obvious contraindication…
Diabetes Insipidus is very common after brain death…incidence is 38-45% according various studies…There is polyuria and hypernatremia due to loss of function of the brain stem and deficiency of ADH..
The key to the management is the fluid and electrolyte replacement and observing the rule of 100…..We need to maintain hydration by giving 5%D or 1/2 N saline depending on the sodium level…SBP around 100mm,PaO2 -100 mm of Hg, Hb – 100g/L, urine output atleast 100 ml pr hour…If the sodium levels are not corrected we need to maintain with Vasopressin 1 U bolus followed by infusion of 0.5 u/hour
Would you accept this donor?
This potential donor is an ECD with age. Between 50 to 60 and a history of CVS accident
increased urine output (polyuria) which may be a sign of central diabetes insipid due to defect in posterior pitutary.
Cerebral salt wasting is suspected.
I shall accept this donation
How do you manage this condition?
Proper fluid and electrolytes replacement. Keeping proper UOP of 1ml/kg /hour .
With LV ejection fraction of at least 45 % using crystalloids .
Desmopressin have no actual outcomes in graft survival
I would accept this donor
He need optimal fluid and electrolytes resuscitation
Yes.
Management.
adequate hydration
monitor serum sodium , serum osmolarity, urine sodium , urine osmolarity.
KIV desmopressin.
I will accept thIs donor but with good management of volume deletion caused by DI
I will gladly accept this donor. After brain death, he has polyuria due to posterior pituitary dysfunction.
He requires fluid resuscitation, electrolyte maintenance, arginine vasopressin/ desmopressin, and adherence to donor management protocols after brain death.
Because there is no contraindication for donation, I will accept this DBD donor.
Proper evaluation of this condition ( Diabetes Insipidus) with good hydration and management of electrolytes.
Desmopressin can be given.
Would you accept this donor?
Yes, I would accept this donor 59 year , DBD, SAH grade 5, S. Cr normal and with poly urea
Diabetes insipidus is common among brain-dead donors and may lead to decreased graft function.
How do you manage this condition?
correction of diabetes inspidus.
Desmopressin can be given to brain-dead donors to limit the harmful effects of diabetes insipidus without any substantial effects to graft function in recipients.
.Fiser DH . Jimenez JF .Wrape V . Woody R
Diabetes insipidus in children with brain death. Crit Care Med. 1987; 15: 551-553
Yes, I will accept this DBD donor because there is no contraindication.
He has polyuria due to diabetes insipidus. So, he needs proper hydration and initiation of desmopressin and control of electrolytes.
There is no contraindication for accepting this donor with brain stem death.
The management includes:
Keeping systolic blood pressure >100mmHg
PaO2 >100mmHg
Hgb concentration> 100g/L
blood sugar 100mg/dL
Regarding polyuria:
Fluids should be replaced to avoid hypovolemia and correct volume status.
Vasopressin is the preferred vasoactive agent to support mean arterial blood pressure and to counteract central diabetes insipidus.
Zirpe K, Gurav S. Brain Death and Management of Potential Organ Donor: An Indian Perspective. Indian J Crit Care Med 2019;23(Suppl 2):S151–S156.
Yes would accept. Donor with good criteria for the transplant: DBD, under 60 years old, without comorbidities that affect the kidney. It would remove the need for biopsy and histopathology from the protocol.
The presence of polyuria secondary to the diabetes insipidus in patients with SAH is expected and does not contraindicate transplantation.
Care for this condition begins with the donor, who must undergo fluid replacement of urinary losses with crystalloids and undergo treatment with desmopress.
Accepting this donor with evidence of DBD, diabetes insipidus can be hopeful for recipients as it can be improved after the use of vasopressin.
Prior exclusion of cerebral aneurysm or history of Autosomal dominant polycystic kidney disease is mandatory.
Management would start by the use of vasopressin as a first-line agent for hemodynamic instability. Donor hypothermia has improved the results regarding renal transplantation. Proper fluid and electrolyte balance to avoid further dehydration and subsequent hemodynamic instability that may cause hazards to renal tissue.
Vasopressin use has been shown to increase procurement yield and is helpful in reducing inotrope use. Based on the fact that the early sign of endocrine failure is diabetes insipidus resulting from depletion of antidiuretic hormone (ADH). The use of a combination of thyroid hormone, corticosteroid, antidiuretic hormone, and insulin seems to be the best approach in these situations to overcome the neuronal cell death associated endocrinopathy.
Reference:
ICU Management of the Potential Organ Donor: State of the Art
Maciel, C.B., Greer, D.M. ICU Management of the Potential Organ Donor: State of the Art. Curr Neurol Neurosci Rep 16, 86 (2016). https://doi.org/10.1007/s11910-016-0682-1
I will accept the donor.
I will manage like CDI.
Would you accept this donor?
· This index donor can be accepted as ECD DBD after he had SAH(grade 5)secondary to cerebral aneurysm. He has excellent renal functions with mild recent increment in Serum creatinine. However it is necessary to exclude ADPKD being associated with cerebral aneurysm.
· It is not uncommon to have loss of posterior pituitary functions(dysfunction of hypothalamic -pituitary axis), central DI due to depletion of AVP, polyuria ,hypernatremia and the production of dilute urine. This may result in in dehydration, AKI and increase risk of DGF
How do you manage this condition?
A) general principle of the “Rule of 100”.
B)Temperature: keep the core temperature >35°C prior to organ donation.
C) DI management:
· Maintain hemodynamic state using enteral and parenteral IV balanced crystalloid solutions (like Ringer’s lactate, Plasmalyte, half normal saline with sodium bicarbonate)
– Inotropic support: if there is no response to fluid resuscitation(Dopamine is the drug of choice)
· If urine output is >4 ml/ kg/hr (refractory cases to fluid resuscitation), treat with vasopressin infusion or DDAVP depending on hemodynamic stability. So, vasopressin infusion can be used in case of low blood pressure while Desmopressin can be given in cases with no hypotension with no substantial effect on graft functions in the recipients
· It is also wise to check and replace other hormonal deficiencies(insulin, steroids and thyroid hormone replacement)
References:
1.Kumar L. Brain death and care of the organ donor. J Anaesthesiol Clin Pharmacol. 2016 Apr-Jun;32(2):146-52
2.BTS guidelines. Transplantation from deceased donors after circulatory death. July 2013.
3. Cristina Capatina, Alessandro Paluzzi, Rosalid Mitchell, Niki Karavitaki. Diabetes Insipidus after Traumatic Brain Injury. J Clin Med. 2015 Jul; 4(7).
yes i accpeted .
He had DI but easy to treat,but better to transplanted in adult case because it need more fluid correction because the DI.
also
(dDAVP), an ADH analog
_ I will accept the donor, with polyurea mostly DI secondary to pituitary dysfunction. Diagnosis requires Na more than 145, serum osmolality more than 300, urine osmolarity less then 300.
-Exclusion of polycystic kidney disease as an association with cerebral aneurysm is required before accepting the potential donor.
_ Management includes:
_ proper correction of diabetes inspidus.
_ correction of the volume status and dehydration by half normal saline or ringer solution to prevent hyoernatremua and it’s deleterious effect on organs especially the kidney.q
_ desmopressin infusion.
_ the target is SBP more than 100 mmHg, random glucose more than 100 mg/dl, UOP 100cc/hour.
-dopamine infusion and L-troxin replacement may be indicated.
*This potential DBD donor consider ECD due to age 59 years old male DBD with SAH (G5) complicating cerebral aneurysm, had polyurea UOP 12 ls; mostly due to
Central DI which account for about upto 80% of these DBD donors due to posterior pituitary function abnormalities and depletion of AVP , characterized by : UOP >4 ml/ kg/ h with s.Na >145 mmol , ser.osmolality >300 mosmol/kg, and low urine osmolality <200 mosmol kg.
*management this condition:
The rule of 100 included : systolic arterial pressure >100 mmHg , uop >100 ml/h (PaO2) >100 mmHg, HB >10 g/dL , good blood sugar controlled target 100mg/dl.
*So; Good hydration with IV Fluids replacement therapy using hypotonic solutions containing to replenish fluid deficit and urinary losses, replace ADH by DDAVP vasopressin should be used in low doses , but if DI persists more than 48hours , desmopressin intra-nasally which is selective action on V2 receptor and a half-life is better indicated. Dopamine infusion if hypotensive. Methylprednisolone 15 mg/kg immediately after diagnosis of brain death and after 24 hour. Insulin 10 U in D50% then infusion to maintain blood glucose around 100 mg/dl . Thyroxin (T4) or Tri-iodothyronin (T3) .T4 improves hemodynamics and prevents cardiovascular collapse.
References:
Robert J. Brown .Polyuria and cerebral vasospasm after aneurysmal SAH. BMC Neurol ,2015; 15: 201
Findlater C, Thomson EM. Organ donation and management of the potential organ donor. Anaesth Intensive Care Med. 2015;16:315–20.
This is ECD kidney as donor age between 50-60years, death due to SAH. Otherwise it is good kidney. But we need to maintain the organs till retrieval, so this polyuria should be managed properly.
So, I will accept the offer.
To manage this donor properly we must follow local guidelines for management of brain death. Special to this case is the polyuria which is due to central diabetes insipidus most probably secondary to posterior pituitary dysfunction. This donor passing 12 liters of urine, so replacement is essential otherwise he may go in to severe hypernatremia, hyperosmolality and dehydration leading to loss of organs, notably the kidneys. So, we have to see serum electrolytes specially serum Sodium and according to water deficit equation will replace fluid with hypotonic fluid (D5% water or half saline) plus the insensible loss and other loses.
To stop this polyuria we need to replace ADH, so will give desmopressin: Vasopressin 1 U bolus followed by an infusion of 0.5-4.0 U/h.
Water deficit = total body water x (Serum sodium -140)/ 140
In addition to replacing urine according to its content of Na and K, according to electrolyte free urine formula= Urine volume-urine volume ( Urine Na+Urine K)/ serum Sodium.
References:
Journal of Anaesthesiology Clinical Pharmacology | April-June 2016 | Vol 32 | Issue 2
Yes, 59 yrs with good kidney function, polyuria , ill look for any other co-morbidity
Working diagnosis of central DI
Urinary water loss should be clamped by administrating desmopressin (dDAVP), and water deficit should be replaced with hypotonic fluids.
regular dDAVP is only prescribed if polyuria persists beyond 48 hours, with ongoing monitoring of pNa and urine volume advised.
48Hannon MJ, Finucane FM, Sherlock M, Agha A, Thompson CJ. Clinical review: disorders of water homeostasis in neurosurgical patients. J Clin Endocrinol Metab. 2012;97(5):1423-1433.
CrossrefCASPubMedWeb of Science®Google Scholar
59 years old male DBD with SAH cerebral aneyssm – with polyarea mostly due to
Central DI.
Hydration of patient
vasopressin DDAVP
this Donor had good renal function with baseline baseline S Cr was 60 µmol/L.
she had brain stem death as she suffered from SAH (grade 5),complicating cerebral aneurysm. I will accept the donor ,ultrasound must be done to ensure absence of PKD which might be associated with cerebral aneurysm.
Increased intracranial pressure (ICP) initially causes an increase in arterial pressure to maintain cerebral perfusion pressure. If ICP continues to increase, then brain herniation ensues with pontine ischaemia and a hyper-adrenergic state.
Pituitary ischaemia and dysfunction of the hypothalamic-pituitary axis leads to diabetes insipidus (DI) creating further fluid loss and electrolyte disturbance.
DI is characterized by a urine output >4 ml kg−1 h with a high serum sodium >145 mmol litre, an increased serum osmolality >300 mosmol kg, and a low urine osmolality <200 mosmol kg.
It occurs in up to 65% of potential donors with brain stem death.
Fluid replacement with enteral or i.v. solutions containing minimal sodium needs to treat both fluid deficit and ongoing losses.
Early use of vasopressin may prevent the need for additional treatment, but if DI persists, desmopressin is indicated.
All anterior pituitary hormones can decrease and hypothyroidism can occur, contributing to multi-organ failure
Vasopressin is givin as follow:1 IU slow i.v. bolus. Infusion up to 2.4 IU h i.v. titrated to arterial pressure ,it is also indicated for hemodynamic instability,but It might cause coronary, renal, and splanchnic vasoconstriction in high doses .
Desmopressin 1–4 μg i.v. bolus. 1–2 μg i.v. 6 hourly.
Our donor DBD with polyuria mainly DI good renal function I will accept this donor and considering as suitable one .
how to manage
according to Brain death and care of the organ donor Lakshmi Kumar Article
Protocols for donor management
The circulatory and biochemical variables are managed by the general principle of the “Rule of 100”
1. Temperature: The aim is to keep the core temperature >35°C prior to organ donation.
2.Fluid management: These patients are often polyuric and dehydrated which is worsened by a vasoplegic state resulting in central volume depletion. Crystalloids are the first choice and balanced salt solutions (Ringer’s lactate, Plasmalyte-A, Ringer’s acetate, half normal saline with sodium bicarbonate) may be superior to normal saline as they do not produce hyperchloremic acidosis. Uncorrected hypernatremia could result in graft losses after liver transplant. Hydroxyethylstarches are contraindicated in organ donors because they can damage renal epithelial cells and cause early graft dysfunction in the transplanted kidneys.
3. Inotropes and cardiovascular system: Dopamine is the first choice of inotrope in hypotension unresponsive to volume and has beneficial effects on the renal graft.
4. Ventilatory management: The principles are along the lines of management of ALI (low tidal volume 6-8 ml/ kg, minimum plateau pressure, lung recruitment).
5. Replacement of hormones after brain death:
a. Vasopressin 1 U bolus followed by an infusion of 0.5-4.0 U/h (desmopressin intranasally has a selective action on the V2 receptors and a half-life varying from 6 to 20 h.
b. Methylprednisolone 15 mg/kg immediately after diagnosis of brain death and 24 th hourly thereafter.
c. Insulin 10 U in 50% dextrose followed by an infusion to maintain blood glucose between 80 and 150 mg.
d. Thyroxine (T4) 20 mcg bolus followed by infusions of 10 mcg/h. Tri-iodothyronine (T3) given as a 4-mcg bolus followed by an infusion of 3 mcg/h. T4 improves hemodynamics and prevents cardiovascular collapse in hemodynamically unstable organ donors.
6.Infection control
Yes I will accept this donor with close follow up to hemodynamic stability
Donor with polyurea developd as result of SAH considered as transient DI
●The major symptoms of central diabetes insipidus (DI) are polyuria, nocturia, and polydipsia. Most patients have a normal or only mildly elevated plasma sodium concentration because concurrent stimulation of thirst minimizes the degree of net water loss. Treatment of this disorder is aimed at decreasing the urine output.
●There are three major therapeutic options:
1- a low-solute (sodium and protein) diet
2-desmopressin (dDAVP), an ADH analog
1-other drugs, including thiazide diuretics.
The choice of therapy varies with the severity of the polyuria.
*Patients with partial DI and mild to moderate polyuria and nocturia may be adequately controlled with a low-solute diet (if acceptable to the patient) and, if necessary, a thiazide diuretic.
Although these modalities also reduce the urine output in patients with marked polyuria and nocturia, desmopressin therapy is usually required for symptom control. Desmopressin can also be used in patients with less severe DI who do not want to comply with a low-solute diet.
The initial aim of therapy with desmopressinis to reduce nocturia, thereby permitting adequate sleep; after this is achieved, one aims for control of the diuresis during the day.
Desmopressin can be administered intranasally
Orally
Subcutaneously
intravenously.
The intranasal preparation should be used initially as not all patients respond to oral therapy.
•For the intranasal preparation, an initial dose of 5 mcg at bedtime can be titrated upward in 5 mcg increments depending upon the response of the nocturia. The usual daily maintenance dose is 5 to 20 mcg once or twice a day.
•For the oral preparation, the initial dose is 0.05 mg (one-half a 0.1 mg tablet) at bedtime with subsequent titration as with the intranasal preparation. The usual daily maintenance dose ranges from 0.1 mg to 0.8 mg in divided doses but may be as high as 1.2 mg/day.
•For the subcutaneous preparation, the usual dose is 1 mcg every 12 hours.
•For intravenous administration (in patients who do not have an adequate response to the subcutaneous preparation), 2 mcg of desmopressinacetate may be given over two minutes; the duration of action is 12 hours or more.
●Desmopressin can lead to water retention and hyponatremia if the urine is concentrated for most of the day. This can usually be avoided by giving the minimum required dose to control the polyuria and not administering another dose until the patient has had a period of brisk diuresis, indicating that the effect of the previous dose of desmopressin had waned.
The serum sodium concentration should be checked at 24 hours after the initiation of desmopressin therapy and patients educated about the symptoms that may be induced by hyponatremia.
Desmopressin therapy should be continued for as long as the patient has central DI.
The duration of central DI varies: DI is permanent in idiopathic disease, improves in some older adult patients with familial disease
In transient type following neurosurgery (usually transsphenoidal), and may be reversible with appropriate therapy in patients with infiltrative diseases.
●Other drugs that may decrease diuresis, but that are rarely used in central DI, include chlorpropamide, carbamazepine and clofibrate, nonsteroidal antiinflammatory drug (NSAID) and thiazide diuretics.
Fluid Management
• Fluid replacement consists of two IV lines of the following:
The Nephrology team in collaboration with the CICU team will set BP, CVP and UOP targets at handover in CICU and at least daily on ward round.
IV line 1:
Insensible losses: 400mL/m2 /day of 0.45% sodium chloride + 5% glucose
IV line 2:
Urine replacement: mL:mL replacement of previous hour urine output.
Fluid options: 0.9% sodium chloride, 0.45% sodium chloride and Plasmalyte
• Glucose free solutions are typically required for urine replacement due to high BSLs.
• 0.45% sodium chloride will need to be ordered in advance.
• Additional fluid bolus are commonly required to meet BP, CVP and UO targets. Patients may require inotropic support for blood pressure if fluids required is excessive.
• This fluid regime is generally continued for the first 48 hours and then a constant IV fluid rate can be used.
references
1-UP TO DATE
2-RENAL TRANSPLANT: IMMEDIATE MANAGEMENT – SCH PRACTICE GUIDELINE
Guideline No: 2018-043 v2 Guideline: Renal Transplant: Immediate Management – SCH
59 year old DBD donor and SAH complicated with aneurysm with good renal function but polyuria
I will accept this donor and manage this case by :
** The general principle of the “Rule of 100”
– SBP ≥100 mmHg
– urine output ≥100 ml/h
– hemoglobin of ≥100 g/L
– PaO2 ≥100 mmHg
– blood sugar targeted at 100% normal.
** keep the core temperature >35°C prior to organ donation
** Fluid management: This patient is polyuric and often dehydrated
So he needs Crystalloids and Ringer’s lactate, may be superior to normal saline
** corrected hypernatremia if found
** Inotropes and cardiovascular system: Dopamine , Nor-adrenaline in doses >0.05 mcg/kg/min
** Ventilatory management
** Replacement of hormones
Vasopressin
Methylprednisolone
Insulin
Thyroxine
Yes its ECD with ,polyuria is common after a SAH and is significantly
associated with cerebral vasospasm.(1)
aggressive fluid therapy to maintain euvolemia and sodium replacement to maintain
serum sodium level.
Refences:
1- Robert J. Brown .Polyuria and cerebral vasospasm after aneurysmal subarachnoid
hemorrhage. BMC Neurol ,2015; 15: 201..
This patient seems to be hypovolemic due to DI resulting from SAH. We need to stop polyuria and prevent hypotension. To keep his volume and blood pressure, we have to use crystalloids, with monitoring of his sodium level solutions other than normal saline may be preferable to avoid hyperchloremia. We need to administer desmopressin iv if available. temporary Dopamine infusion (if hypotensive).
This donor can be accepted safely because supportive treatment will reverse AKI.
Assessment of the donor’s kidney
· Clinical data: 59-year-old male DBD with no history of DM and Hypertension
· Laboratory and radiological data: with excellent kidney function in the form of (S Cr was 75 µmol/L and UOP the last 24h was 12 L
· Pre-implantation biopsy (Remuzzi score), in the current patient will add nothing since there is no history of chronic kidney disease
So, yes I will accept this donor
this polyuria is seen commonly in DBD (46-86%) due to posterior pituitary function abnormalities and depletion of AVP (1).
How do you manage this condition?
managed by the general principle of the “Rule of 100”.
This can be achieved by
· Fluid management: These patients are often polyuric and dehydrated and should be corrected by Crystalloids are the first choice and balanced solutions like Ringer’s are preferred to normal saline to avoid hyperchloremic acidosis.
A- Vasopressin 1 U bolus followed by an infusion of 0.5-4.0 U/h
B- Methylprednisolone 15 mg/kg bolus and 24th hourly thereafter.
D-Thyroxine (T4) 20 mcg bolus followed by infusions of 10 mcg/h.
Reference
1-Verbalis JG, Goldsmith SR, Greenberg A, Korzelius C, Schrier RW, Sterns RH, et al. Diagnosis, evaluation and treatment of hyponatremia: Expert panel recommendations. Am J Med. 2013;126(Suppl 10):S1–42.
2. Upadhyay A, Jaber BL, Madias NE. Incidence and prevalence of hyponatremia. Am J Med. 2006;119(Suppl 1):S30–5
3-. Wijdicks EF, Varelas PN, Gronseth GS, Greer DM, American Academy of Neurology. Evidence-based guideline update: Determining brain death in adults: Report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2010;74:1911-8.
This is a case of DBD with polyuria and 25% increase in serum creatinine from baseline.
‘This implies that potential donor has developed endocrine dysfunction post brain death. He has developed central DI which is causing polyuria and patient has some dehydration hence creatinine is creeping up.
I will start depression to reduce urine output, correct if hypernatremia develops with adequate fluid supplementation.
I will go ahead with transplantation but will keep induction immunosuppression high and CNI low for initial few days post transplantation as graft kidneys might have suffered some ATN secondary to hypovolemia.
DBD with normal baseline & on admission serum creatinine, can accepted as a potential donor after excluding polycystic kidney disease, infection or any other contra-indication for donation.
But we should consider the early loss of endocrine function after DBD especially posterior pituitary function leading to ADH deficiency in 80% of patient & development of DI in 77% of DBD cases which presented as polyuria & hypernatremia.
This patient had DI & he should treated with desmopressin 1 u as bolus & maintained on 0.5-4u /hr as infusion with IV fluid to maintain good hydration.
References:
Yes I will accept the donation with reviewing his medical records in details for any previous comorbidities and chronic diseases.
Management of this patient is by the rule of 100 including PaO2> 100 mmHg, BP > 100 mmHg, HB > 100 gm\l, urine output > 100 cc\hr and blood sugar of 100% normal values.
· Would you accept this donor?
Yes I will accept the donor as 59 years after DBD
S Cr was 75 µmol/L
Good urine output ( But he is associated with polyuria )
DD of Polyuria
DI : it is caused by a lack of anti-diuretic hormones secreted by the posterior pituitary gland
Brain salt losing
hyperglycemia (common endocrine change in brainstem-dead patients due to reduced insulin concentrations and insulin resistance )
the use of a diuretic or Osmotherapy
How do you manage this condition?
The “rule of 100 included :
systolic arterial pressure >100 mmHg
urine output >100 ml/hr
(PaO2) >100 mmHg,
haemoglobin concentration >10 g/dL
blood sugar good controlled
Volume expansion and fluid management
Crystalloids: should be used to avoid hypernatremia (associated DI). Lactated Ringer’s solution and half tonic saline (0.45%) are frequently used
Normal saline may cause hyperchloremic acidosis
You can use albumin solutions (4% and 20%) to limit back on the amount of fluid you supply.
Hypotension:
volume expansion, vasopressors, and inotropes, and hormonal replacement
Temperature Management
all patients with hypothermia should receive surface warming to keep their temperature above 35.8°C.
Vasoactive agents
When basic fluid resuscitation is insufficient to restore BP and CO, patients need extra vasoactive medications.
Noradrenaline, adrenaline, vasopressin, dopamine, and/or dobutamine are frequently administered alone or in combination, depending on local guidelines.
Vasopressin manages DI very well and lessens the hemodynamic necessity for employing various catecholamines.
Combined hormonal therapy
the combination of methylprednisolone, vasopressin, and triiodothyronine is still debatable, some researchers have suggested that it may enhance the quality of retrieved organs and hemodynamic stability in brain-dead individuals.
High dosages of corticosteroids may improve the quality of donor organs and post-transplant graft function by reducing brain death-induced inflammation and by modulating the immune response.
Insulin :
due to hyperglycemia resulting from insulin resistance and gluconeogenesis.
Anti-diuretic hormone :
if associated with DI as may result in hypovolemia, hyperosmolality, hypernatremia, hypermagnesemia, hypokalemia, hypophosphatemia, and hypocalcemia
References :
Bugge JF. Brain death and its implications for management of the potential organ donor. Acta Anaesthesiol Scand. 2009;53:1239–50.
Wood KE, Coursin DB. Intensivists and organ donor management. Curr Opin Anaesthesiol. 2007;20:97–9.
Findlater C, Thomson EM. Organ donation and management of the potential organ donor. Anaesth Intensive Care Med. 2015;16:315–20.
Kotloff RM, Blosser S, Fulda GJ, Malinoski D, Ahya VN, Angel L, et al. Management of the potential organ donor in the ICU: Society of Critical Care Medicine/American College of Chest Physicians/Association of Organ Procurement Organizations Consensus Statement. Crit Care Med. 2015;43:1291–325.
I can accept that donor with reviewing his data to evaluate comorbidities especially APKD.
Management: Rule of 100 can be implemented ; SBP ≥100 mmHg., urine output ≥100 ml/h, Hb of ≥100 g/L,PaO2 ≥100 mmHg and blood sugar targeted at 100% normal.
Hormonal replacement is needed for better utilization heart and lungs for not affecting other organs:
-.Vasopressin 1 U bolus then infusion of 0.5-4.0 U/h and a half-life varying from 6 to 20 h to replace the hormonal deficiency and improve polyuric status.
.Methylprednisolone 15 mg/kg following brain death and then 24th hourly.
.Insulin 10 U in 50% dextrose followed by infusion to achieve blood glucose between 80-150 mg.
.Thyroxine ;T4 20 mcg bolus followed by infusions of 10 mcg/h. Tri-iodothyronine T3 given 4-mcg bolus then infusion of 3 mcg/h.T4 supports haemodynamic status and prevents collapse in unstable donors.
59-year-old DBD from SAH had cerebral aneurysm, having Polyuria and elevated sr creatinine. Patient suffering central DI secondary to SAH.
I will accept the donor.
I will hydrate with hypotonic fluid to avoid dehydration with a target mean arterial pressure of at least 60 mmHg, urine output of > 1 ml/kg/hour
In presence of persistent hypotension, intravenous AVP 0.01-0.04 IU/min should be given.
Correction of other electrolyte imbalances (potassium, magnesium, phosphorus ) should be done.
Use of desmopressin has no effect on graft outcomes
Guesde R et al showed no significant differences between the two groups of brain-dead donors in which one group received desmopressin and the other did not . The only difference is final diuresis, which was lower in the desmopressin group.
References
Latifi M, Bagherpour F, Rahban H, Pourhossein E, Dehghani S. Brain death hormone therapy and Graft survival: A systematic review of the literature. Transplantation Reports 2022;7:100098.
Guesde R, Barrou B, Leblanc I, Ourahma S, Goarin JP, Coriat P, Riou B. Administration of desmopressin in brain-dead donors and renal function in kidney recipients. Lancet. 1998 Oct 10;352(9135):1178-81
rule of 100 targets , target blood pressure >100 mmHg, PaO2 >100 mmHg, Hgb >100 gm/l & blood sugar of 100% normal value.
1. Temperature: The aim is to keep the core temperature >35°C prior to organ donation.
2. Fluid management: . Crystalloids are the first choice and balanced salt solutions (Ringer’s lactate, Plasmalyte-A, Ringer’s acetate, half normal saline with sodium bicarbonate)
3. Inotropes and cardiovascular system: Dopamine is the first choice of inotrope in hypotension unresponsive to volume and has beneficial effects on the renal graft.
4. Ventilatory management: The principles are along the lines of management of ALI (low tidal volume 6-8 ml/ kg, minimum plateau pressure, lung recruitment).
5. Replacement of hormones:
a. Vasopressin 1 U bolus followed by an infusion of 0.5-4.0 U/h
b. Methylprednisolone 15 mg/kg immediately after diagnosis of brain death and 24th hourly thereafter.
c. Insulin 10 U in 50% dextrose followed by an infusion to maintain blood glucose between 80 and 150 mg.
d. Thyroxine (T4) 20 mcg bolus followed by infusions of 10 mcg/h. Tri-iodothyronine (T3) given as a 4-mcg bolus followed by an infusion of 3 mcg/h. T4 improves hemodynamics and prevents cardiovascular collapse in hemodynamically unstable donors
(Brain death and care of the organ donor Lakshmi Kumar , Journal of Anaesthesiology Clinical Pharmacology | April-June 2016 )
A potential donor,59-year-old male DBD donor who suffered from SAH (grade 5) complicating cerebral aneurysm. Her baseline S Cr was 60 µmol/L. On admission, S Cr was 75 µmol/L, he also passed 12 L over the last 24 hours.
Would you accept this donor?
Yes; i would accept this potential donor kidneys, after detailed look at his medical record, if any proteinuria, hematuria, nephrolithiasis, ADPCKD (polycystic kidney disease), and if any othe comorbidities such as history of HTN, DM, or cardiovascular disease.
How do you manage this condition?
Management of donor : Rule of 100’s = target blood pressure >100 mmHg, UOP >100/hr, Hgb >100 gm/l, blood sugar of 100% normal value, and PaO2 >100 mmHg.
Fluids: Crystalloids are the first choice and balanced salt solutions (Ringer’s lactate, Plasmalyte-A, Ringer’s acetate, half normal saline with sodium bicarbonate),, special concern in our case that might has DI= diabetes insipidus with water loss, in order to overcome hypernatremia, vassopressin 1U given then infusion of 0.5-4 U/hr.
Ventilatory management: low tidal volume of 6-8 ml/kg,the lowest FiO2 applied, lower PEEP, and restrictive fluid strategy.
Hormonal management: IV Methylprednisolone 15 mg/kg at the diagnosis of brain death and 24 hours doses thereafter. IV Thyroxin 20 mcg stat then 10 mcg/hr. infusion.
Insulin in dextrose maintaining normal blood sugar of 80-150 mg/dl.
Infectious screen and management : Hepatitis B and C, CMV, HIV, HSV, EBV….. etc.
References:
[1] Kumar L. Brain death and care of the organ donor. J Anaesthesiol Clin Pharmacol. 2016 Apr-Jun;32(2):146-52. doi: 10.4103/0970-9185.168266. PMID: 27275040; PMCID: PMC4874065.
[2] Andrews PA, Burnapp L, Manas D; British Transplantation Society. Summary of the British Transplantation Society guidelines for transplantation from donors after deceased circulatory death. Transplantation. 2014 Feb 15;97(3):265-70. doi: 10.1097/01.TP.0000438630.13967.c0. PMID: 24448588.
Dear Dr Alshaikh,
Your point-wise reply is excellent that highlights very practical issues.
Would you accept this donor?
I would accept this donor provided ADPKD was excluded, as association with cerebral aneurysm is common.
a) The donor is SCD.
b) The kidney function is normal at baseline and on retrieval.
c) The polyuria is explainable by the possibility of central DI.
How do you manage this condition?
Protocols for donor management
“Rule of 100”:
a) targets of SBP ≥100 mmHg.
b) urine output ≥100 ml/h.
c) hemoglobin of ≥100 g/L.
d) PaO2 ≥100 mmHg.
e) blood sugar targeted at 100% normal.
Elements of donor management are:
1. Temperature: The aim is to keep the core temperature >35°C prior to organ donation.
2. Fluid management: Crystalloids are the first choice and balanced salt solutions (Ringer’s lactate, Plasmalyte-A, Ringer’s acetate, half normal saline with sodium bicarbonate) may be superior to normal saline as they do not produce hyperchloremic acidosis. Hydroxyethylstarches are contraindicated in organ donors because they can damage renal epithelial cells and cause early graft dysfunction in the transplanted kidneys.
3. Replacement of blood and blood products could follow guidelines for the care of the critically ill and a hemoglobin of 10 g/L could improve tissue oxygenation indices.
4. Inotropes and cardiovascular system: Dopamine is the first choice of inotrope in hypotension unresponsive to volume and has beneficial effects on the renal graft. Nor-adrenaline in doses >0.05 mcg/kg/min resulted in impaired cardiac contractility in transplanted hearts and in particular impairment of right ventricular performance.
5. Ventilatory management: The principles are along the lines of management of ALI (low tidal volume 6-8 ml/ kg, minimum plateau pressure, lung recruitment).
6. Replacement of hormones after brain death: Standardization of hormone therapy after brain death in combination with a central venous pressure <10 mmHg significantly improved utilization of the heart and lungs for transplant without affecting other organ systems. The recommended replacements are:
a) Vasopressin 1 U bolus followed by an infusion of 0.5-4.0 U/h.
b) Methylprednisolone 15 mg/kg immediately after diagnosis of brain death and 24th hourly thereafter.
c) Insulin 10 U in 50% dextrose followed by an infusion to maintain blood glucose between 80 and 150 mg.
d) Thyroxine (T4) 20 mcg bolus followed by infusions of10mcg/h.Tri-iodothyronine(T3)given as a 4-mcg bolus followed by an infusion of 3 mcg/h. T4 improves hemodynamics and prevents cardiovascular collapse in hemodynamically unstable organ donors.
You point-wise reply is excellent.
Would you accept this donor?
Yes I will accept this donors.
I will rule out APKD as there is association with cerebral aneurysms. Polyuria is due to posterior pituitary insult due to brain death. This has led to loss of function and ADH. Diabetes insipidus can be managed by fluid replacement and Desmopressin.
How do you manage this condition?
Maintain core temperature > 35C
Will follow the rule of 100
Restoration of circulatory volume is the key to protect vital organs that can be donated. Adequate volume replacement without overload is essential.
Fluid replacement can be done with crystalloids. Ringer lactate is better than isotonic saline as less risk of hyerchloremic metabolic acidosis.
If there is still hypotension in spite of fluid resuscitation then dopamine may improve organ perfusion.
Follow the principle of ALI in ventilatory management
Hormonal replacement–
Thyroxine 20 mcg bolus and then 10 mcg /hr
Insulin 10 units in 50% dextrose followed by infusion- keep sugars between 8-150 mg.
Methylprednisolone 15 mg / kg stat and then after every 24 hours
Vasopressin 1U bolus and then infusion- 0.5-4 U/hr.
Reference
Kumar L. Brain death and care of the organ donor. J Anaesthesiol Clin Pharmacol. 2016 Apr-Jun;32(2):146-52
Your approach is logical.
Thank you Prof Ajay
– This donor is 59 y old DBD with central diabetes insipidus due to SAH causing polyuria, his creatinine is acceptable .
Yes I will accept him after management.
– Desmopressin can be administered as desmopressin as 1 microg bolus every 2 h to brain-dead donors to decrease the harmful effects of diabetes insipidus without any substantial effects to graft function in recipients.
A study by Guesde R et al showed no significant differences between the two groups of brain-dead donors where one group received desmopressin and the other did not , except for final diuresis, which was lower in the desmopressin group than among controls.
On the other side a study be Hirschl demonstrated that desmopressin use during organ procurement is associated with a higher rate of primary non-function of renal allografts.
Rech et al declared that desmopressin use was not associated with better kidney graft outcomes , but it is safe and useful to limit the harmful effects of profuse polyuria, decreasing the need for large volume infusions and preventing hemodynamic collapse . Studies have suggested the use of colloid solutions as an option to avoid the infusion of large volumes to treat hypovolemia.
Pennefather et al recommended considering the use of a low dose Arginine vasopressin infusion in potential organ donors as it’s use in a low dose infusion enabled the inotrope use to be reduced because in AVP treated group, plasma hyperosmolality decreased, blood pressure increased , inotrope use decreased , and cardiac output was maintained.
Reference
-Guesde R, Barrou B, Leblanc I, Ourahma S, Goarin JP, Coriat P, Riou B. Administration of desmopressin in brain-dead donors and renal function in kidney recipients. Lancet. 1998 Oct 10;352(9135):1178-81
– Hirschl MM, Matzner MP, Huber WO, Binder WO, Röggla G, Derfler K, Mühlbacher F, Laggner AN. Effect of desmopressin substitution during organ procurement on early renal allograft function. Nephrol Dial Transplant. 1996 Jan;11(1):173-6.
– Rech, Tatiana H.1; Moraes, Rafael B.1; Crispim, Daisy2; Czepielewski, Mauro A.2; Leitão, Cristiane B.2,3. Management of the Brain-Dead Organ Donor: A Systematic Review and Meta-Analysis. Transplantation Journal: April 15, 2013 – Volume 95 – Issue 7 – p 966-974
– Pennefather, Stephen H.2; Bullock, Robert E.2; Mantle, David4; Dark, John H.5. USE OF LOW DOSE ARGININE VASOPRESSIN TO SUPPORT BRAIN-DEAD ORGAN DONORS. Transplantation: January 15, 1995 – Volume 59 – Issue 1 – p 58-62
Dear Dr Doaa,
I like the scientific contents of your reply. Please type headings and subheadings in bold or underline so that it is easier to read.
59-year-old male
DBD from SAH
Polyurea
mild increment in serum creatinine level
The high volume of urine can be explained by DI secondary to SAH.
Diabetes insipidus is a relatively uncommon abnormality of water homeostasis resulting from the excess production of hypotonic urine. It is classified as central or nephrogenic, based on its aetiology as an abnormality in antidiuretic hormone production or release,
ADH sensitivity, or the aquaporin channel gene. The clinical presentation of DI includes hypotonic polyuria and polydipsia, with urine output exceeding 50 mL/kg body weight/24 hours, and excessive drinking of >3 L/day.
Central DI, the more common form of DI, is classified as traumatic or non-traumatic.
The diagnosis of central DI requires an intact renal function to manifest polyuria.
I will accept the donor.
References:
THat is a good reply, dear Dr Taee.
thank you
I’ll accept this donor, with special caution.
As there is brain aneurysm, so need to exclude ADPKD.
There is polyuria due to DI, as a consequence of brain stem death.
So, vasopressin replacement is needed accordingly.
Yes, Dr Ansary.That is a sensible reply, but without any evidence to support your arguments.
This donor is acceptable ,although he has central DI which is for sure associated with DBD ,just we need to be sure of all hormonal status and replacement should be done.
We need to diagnose the ID and early vasopressin administration .
we need to screen this donor by doing US to R/O APKD in association with SAH.
if he has no APKD ,I will accept the donor .
Since it is a good candidate for organ donation we need to optemize the rule of 100:
Yes, Dr Rihab.That is a sensible reply, but without any evidence to support your arguments.
Case of 59 years old DBD suffered from SAH complicating aneurysm with normal renal function and poly urea.
first this young patient with complicating aneurysm with no co morbidities I will do u/s to role out APKD(if kidney is normal iwill accept this donor).
pateint has polyurea need to confirm the cause ,check the blood sugar,
or has diabetus insipidus which is diagnosis by:
urine out put more than 4 l per 24 hours.
serum sodium more than 145mmol/l
serum osmolity more than300 mosmol/kg and low urine osmolity less than 200mosmol/kg..
management of central DI in DBD:
ID occurs up to 65%of potential donor.
fluid replacementi.v fluid contain minimal sodium needs to treat both fluid deficit and on going losses.
early use of vasopressin may prevent the need for additional treatment.
if DI persist decompression is indicated.
all hormones of anterior pituitary should be test and replacement includedT3 (thyroid hormones),Methylprednosolne ,insulin ,vassopressin and desmopression.
References
1National Health Service Blood and TransplantOrgan donation weekly statistics, May 2011 Available from http://www.organdonation.nhs.uk/ukt/statistics (accessed 30 May 2011)
2Organ donation and transplantation policy options at EU level. 27 June 2006. http://ec.europa.eu/health/ph_threats/human_substance/oc_organs/consultation_paper.pdf (accessed 30 May 2011)
3Rosendale JD, Chabalewski FL, McBride MA, et al. Increased transplanted organs from the use of a standardized donor management protocol, Am J Transplant, 2002, vol. 21 (pg. 550-7)
Dear Dr Malik
I like the scientific contents of your reply. Please type headings and subheadings in bold or underline so that it is easier to read.
This is a 59 year old donor after brainstem death.
His serum creatinine is acceptable, the problem is polyuria.
It is due to diabetes insipidus.
The posterior pituitary function is lost early in brain death with occurrence of diabetes insipidus with polyuria and hypernatremia.
Arginine vasopressin and desmopressin can be given as replacements.
So, I would accept this donor.
This case can be managed as :
“Rule of 100”
I would maintain a
Kumar L. Brain death and care of the organ donor. J Anaesthesiol Clin Pharmacol 2016;32:146-52.
Thankyou
Donor 59 years of age, male, DBD form SAH 2nd to cerebral aneurysm with a baseline creatinine of 60 µmol/L, and on admission was 75 µmol/L with a urine output of 12 liters of urine over 24 hours.
In this case, I will accept the patient as a donor. The patient likely has Diabetic Insipidus likely 2nd to the SAH. It is known that during DBD there are hormones that become insufficient. From a source, it says that in patients with brain death, there is posterior pituitary insufficiency and as such can cause DI due to Anti-Diuretic hormone insufficiency(1). This change causes polyuria and hypernatremia. There are other hormones that can be affected like thyroid hormones like low T3 and T4 and others.
Since the patient is a good candidate for organ donation, there are measures that need to be taken to ensure proper graft perfusions.
1) Ensure fluids and electrolytes control. Due to the high diuresis, the patient will need proper hydration to maintain blood pressures MAP above 60 mmHg, to ensure cardiac function and good renal flow.
2) Despite fluid resuscitation, and BP remaining low inotropes can be given.
3) Hormonal therapy must be given to ensure DI is managed that is AVP intravenously.
4) Ensure that there are no electrolyte imbalances and if present must be corrected.
5) Ensure saturation above 100 mmHg
6) Haemoglobin above 10
7) Regulate glycemia levels.
8) Ensure body temperature is above 35 degrees Celsius
9) Other hormones can be given life thyroxin, steroids like methyl prednisone
10) Ensure there are no infections
References:
1. Choi YS, Na S, Kang Y, Koh SO. Hormonal Changes of the Brain-Dead Organ Donors: A 3-Year Experience. Vol. 23. 2008.
Yes, I would accept this man as a donor
He has central DI which is common disorder with brain hemorrhage
– Volume resuscitation with NS
– Support bp
– Accurate fluid chart
– assess blood sugar
– Hormonal assay to assess other hormones
– Hormonal replacement
– CVP line if possible
One of the most common complications after brain death is the hormonal deficiencies like DI , followed by other hormones deficiency like hypothyroidism, hyperglycemia and adrenocortical deficiency.
I will accept donation from this ECD after excluding of the cystic renal disease , and after correcting the following:
Thankyou
59-year-old male DBD donor, SAH (grade 5) complicating cerebral aneurysm, S Cr was 60 µmol/L. On admission, S Cr was 75 µmol/L, he also passed 12 L over the last 24 hours.
Would you accept this donor?
Yes , I will accept him for donation after excluding ADPKD as association with cerebral aneurysm, because his accepted renal function with no past medical history.
He is a case of DBD associated with polyuria which is common due to loss of posterior pituitary function loss of ADH , lead to DI with polyuria and hypernatremia .
How do you manage this condition?
Managing and care of DBD donor is considering harmony protocol to care all the organ donor by care of Cardiovascular system, Respiratory system, Systemic inflammatory response and Endocrine system, stress and metabolic responses which we will focus on it here .
Mainly we need hormonal replacement to improve utilization of the heart and lungs for transplant without affecting other organ systems such as:
A-Vasopressin 1 U bolus followed by an infusion of 0.5-4.0 U/h (desmopressin intranasally has a selective action on the V2 receptors and a half-life varying from 6 to 20 h to replace the hormonal deficiency and correct polyuric status in our case.
B-Methylprednisolone 15 mg/kg immediately after diagnosis of brain death and 24th hourly thereafter.
C-Insulin 10 U in 50% dextrose followed by an infusion to maintain blood glucose between 80 and 150 mg.
D-Thyroxine (T4) 20 mcg bolus followed by infusions of 10 mcg/h. Tri-iodothyronine (T3) given as a 4-mcg bolus followed by an infusion of 3 mcg/h. T4 improves hemodynamics and prevents cardiovascular collapse in hemodynamically unstable organ donors.
References:
1-Kumar L. Brain death and care of the organ donor. J Anaesthesiol Clin Pharmacol. 2016;32(2):146-152. doi:10.4103/0970-9185.168266.
2-Wood KE, Becker BN, McCartney JG, D’Alessandro AM, Coursin DB. Care of the potential organ donor. N Engl J Med 2004;351:2730-9.
3-Salim A, Vassiliu P, Velmahos GC, Sava J, Murray JA, Belzberg H, et al. The role of thyroid hormone administration in potential organ donors. Arch Surg 2001;136:1377-80.
Thankyou well done
I will accept him as a donor.
This potential donor developed diabetes insipidus. Development of diabetes insipidus is common. Failure to achieve cardiovascular stability will lead to rapid deterioration in organ function, and cardiac arrest. Active donor management can prevent this. Rapid restoration of circulating volume without overload is essential. Restoring vascular tone with drugs such as vasopressin is helpful. Suitable donor cardiovascular goals may be less difficult to achieve than previous therapeutic targets. Flow monitoring facilitates rapid titration of therapies, and should be strongly considered at an early stage. When goals are achieved without high dose catecholamine infusions, the chance of donor hearts being transplantable increases.
References: Shemie et al. ‘Organ donor management in Canada: recommendations of the forum on Medical Management to Optimize Donor Organ Potential.’ CMAJ (2006) vol. 174 (6) pp. S13-32 Mascia, L., I. Mastromauro, et al. (2009)
Thankyou
Would you accept this donor?
-Yes ,I would accept this donor.
– The endocrine responses of the body are lost with brain death. The posterior pituitary function is lost early in brain death with occurrence of diabetes insipidus with polyuria and hypernatremia. Arginine vasopressin and desmopressin can
be given as replacements.
How do you manage this condition?
I manage this donor by:
1.The circulatory and biochemical variables are managed by the general principle of the “Rule of 100”suggesting targets of SBP ≥100 mmHg, urine output ≥100 ml/h, hemoglobin of ≥100 g/L, PaO2 ≥100 mmHg and blood sugar targeted at 100% normal.
2.Other elements of donor management are :
1. Temperature: The aim is to keep the core temperature >35°C prior to organ donation.
2. Fluid management: The patients is polyuric and dehydrated .Crystalloids are the first choice and balanced salt solutions (Ringer’s lactate, Plasmalyte-A, Ringer’s acetate, half normal saline with sodium bicarbonate) may be superior to normal saline as they do not produce hyperchloremic acidosis
3. Inotropes and cardiovascular system: Dopamine is the first choice of inotrope in hypotension unresponsive to volume and has beneficial effects on the renal graft.
4. Ventilatory management: The principles are along the lines of management of ALI (low tidal volume 6-8 ml/ kg, minimum plateau pressure, lung recruitment).
5. Replacement of hormones :
a. Vasopressin 1 U bolus followed by an infusion of 0.5-4.0 U/h .
b. Methylprednisolone 15 mg/kg immediately after diagnosis of brain death and 24th hourly thereafter.
c. Insulin 10 U in 50% dextrose followed by an infusion to maintain blood glucose between 80 and 150 mg.
d. Thyroxine (T4) 20 mcg bolus followed by infusions of 10 mcg/h.
Reference:
Lakshmi Kumar. Brain death and care of the organ donor.
Very good well done
what are the potential risks to the graft?
Diabetes insipidus can lead to dehydration and AKI. AKI in kidney donor, which increases the risk of delayed graft function (DGF), may not by itself jeopardize the short- and long-term outcome of transplantation.