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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1739_Библиотеки_им_академика_М_И_Перельмана.pdf
84
A Simple Introduction to Organ Transplant
Dr Gopi Ayyaswamy
General Table of Normal Values
• Sodium (Na): 136–142 mEq/L (mmol/L)
• Magnesium (Mg): 1.5–2.3 mg/L (0.65–1.05 mmol/L)
• Potassium (K): 3.5–5.0 mEq/L (mmol/l)
• Phosphorous (Phos): 2.3–4.7 mg/dL (0.74–1.52 mmol/L)
• Chloride (Cl): 96–106 mEq/L (mmol/L)
• Ionized calcium (Ca
++
): 2.3–2.54 mEq/L (1.15–1.27 mmol/L)
• Bicarbonate (HCO
3
): 21–28 mEq/L (mmol/L)
Note: These values serve as the general reference range for normal electrolyte levels.
Electrolyte Therapy
Sodium (Na) Therapy
Hypernatremia–treat Na > 150 mEq/L
1. With polyuria (>250 cc of urine above intake per hour) see Guideline:
Polyuria.
2. Without polyuria—give 1 liter 0.2% saline as rapid infusion and replace
urine output cc/kg/hr with 0.2% saline. Assure that all medications are
mixed in 0.45% or 0.2% saline if pharmaceutically possible and that any
maintenance IV is D5% 0.2% saline. Avoid use of diuretics.
Hyponatremia–treat for serum Na < 133 mEq/L
a. Mix all medications in 0.9% saline (normal saline) if pharmaceutically
possible. Change maintenance IV to D5 0.9% saline.
b. If hyperglycaemia is present, the serum Na may be low.
c. Because of the high blood glucose and if blood sugar > 300, a
“corrected” serum Na may be calculated by adding to the measured Na:
1.6 mEq for each 100 gm/dl of blood glucose above 100. See Guideline:
Hyperglycaemia and treat.
d. If Na < 128 mEq/L give 3% NaCl per infusion (central line preferred)
at 40 cc/hr × 3 hours.
e. If Na remains < 133 mEq/hr after 3% NaCl infusion, consult physician/
intensivist.
Potassium (K)
Hyperkalemia—treat serum K ≥ 5.8 mEq/L
Medical Issues and Management
85
Dr Gopi Ayyaswamy
a. Note: Do not treat K if laboratory reports specimen
b. “Hemolyzed”—send a new specimen for testing.
c. Assure all K removed from current infusions
d. Repeat serum K q 1 hour
e. Give IV:
• 50 cc of 50% dextrose (D50) (one pre-lled syringe)
• 15 units regular humulin insulin
• 1 amp NaHCO
3
(44 or 50 mEq via pre-lled syringe)
• K > 5.8 mEq/L after above intervention.
Hypokalemia—treat < 3.4 mEq/L
a. Delay administration of any diuretic.
b. Give 20 mEq KCl over 1 hour (central line preferred) as:
• Serum K < 3.4 mEq/L: 2 doses
• Serum K < 3.1 mEq/L: 3 doses
• Serum K < 2.9 mEq/L: 4 doses
• If K remains > 2.9 < 3.8 mEq/L—repeat above
• If K remains < 3.2 mEq/L, thereafter care to
• Ensure >20 µg/L of potassium infusion to prevent arrhythmia related
death.
Chloride (Cl)—not independently treated.
Bicarbonate (HCO
3
)—not independently treated
Magnesium (Mg)
a. Hypermagnesemia—not independently treated
b. Hypomagnesemia—treat Mg < 1.5 mg/d
• Administer 4 grams magnesium sulfate (MgSO
4
) over 2 hours—repeat
as indicated by subsequent laboratory assessments to maintain above
goal levels.
• If Mg remains < 1.5 mg/dl after 8 gm MgSO
4
.
86
A Simple Introduction to Organ Transplant
Dr Gopi Ayyaswamy
Phosphorus (P)
a. Hyperphosphatemia—not independently treated.
b. Hypophosphatemia—treat serum P < 2.2 mg/dl (0.71 mmol/L)
• Give 30 mmol potassium or sodium phosphate over 3 hours and
repeat (total 2 doses)
• If P remains < 2.2 mg/dl (0.71 mmol/L) after 60 mmol sodium or
potassium phosphate given.
Calcium (Ca)
Note: Measure and treat only the ionized calcium value.
a. Hyper-ionized calcemia—not separately treated. Withhold additional
calcium
b. Hypo-ionized calcemia—treat <4.4 mg/dl or <2.1 mEq/L or <1.1
mmol/L
• Give 10 cc 10% solution of calcium gluconate slow IV push.
• Re-measure ionized Ca in 1 hour
• Repeat if ionized Ca is low
• If the ionized Ca remains low after 20 cc, 10% calcium gluconate is given.
Polyuria
Excessive urine production, known as polyuria, can have serious
consequences such as decreased blood volume and inadequate blood ow
to donated organs. There are several possible causes of polyuria, including:
1. Normal diuresis following previous uid administration.
2. Osmotic diuresis due to previous mannitol therapy or ongoing high
blood sugar levels.
3. Diuresis caused by prescribed diuretic medications, and
4. Diabetes insipidus. Only physiological diuresis does not lead to low
blood pressure, whereas the other forms can potentially cause it. If a
donor shows signs of both low blood pressure and polyuria, follow the
guidelines below while also referring to the “hypotension” guideline.
The desired urine output goal is 75–150 cc per hour.
Medical Issues and Management
87
Dr Gopi Ayyaswamy
Initial Assessment
a. Check blood sugar levels through laboratory or nger stick measurement.
Blood glucose levels above 200 mg/dl can contribute to polyuria.
Consult the “glucose management” guideline for further guidance.
b. Discontinue any prescribed diuretic therapy.
c. Calculate the recent balance between fluid intake and output and
adjust the intake to be 100 ml per hour less than the total output.
For example, if the average urine output over the last 3 hours was
around 400 ml per hour, adjust the total IV uid intake to be approxi-
mately 300 ml per hour.
d. Monitor serum sodium and glucose levels every 2 hours.
e. If the sodium level is above 148 mEq/L, assume excessive loss of free
water has occurred and proceed with the treatment plan outlined
below.
f. If the last measured serum sodium level falls within the range of
135–147 mEq/L, observe the urine output and regularly measure serum
sodium levels. Maintain uid intake at a level 100 ml per hour lower
than the urine output.
Treatment
a. Adjust intake to be 100 cc less than output until intake and output are
balanced. Once they are equal, maintain intake equal to output.
b. If the urine output exceeds the IV intake by more than 250 cc over
the past 2 hours and the last measured serum sodium level is above
145 mEq/L, administer 1 µg of intravenous desmopressin (DDAVP).
Additionally, replace each hour’s urine output with an equal amount
of 0.2% saline solution (without dextrose).
c. If the urine output has not decreased to less than 200 ml above the intake
level within the next hour (urine output remains more than 200 ml above
uid intake), administer an additional 1 µg of DDAVP intravenously.
d. If the urine output has not decreased to less than 200 cc above the IV
intake level (urine output remains more than 200 ml above uid intake),
and the sodium level has not fallen below 146 mEq/L within 2 additional
hours, consult a physician/intensivist.
88
A Simple Introduction to Organ Transplant
Dr Gopi Ayyaswamy
Acid–Base Treatment
In the monitoring and treatment of donors, the main focus is on maintaining
the arterial pH within the range of 7.35 to 7.45. The adjustment of arterial
carbon dioxide pressure (PaCO
2
) is done to normalize the arterial pH,
as there are limited primary effects of hypocarbia or hypercarbia. The
guideline for mechanical ventilation provides information on how to
modify the mechanical ventilator to change the PCO
2
and, consequently,
the pH.
Assessment
• Acidosis: Before making any adjustments to the mechanical ventilator
as recommended in the mechanical ventilation guideline, review the
arterial blood gas (ABG) measurement. Evaluate the base excess (BE) or
base decit (BD) values provided in the ABG results. If the BE is more
negative than –6 or the BD is more positive than +6, it is likely that
metabolic acidosis is present.
• Alkalosis: Similarly, review the ABG prior to making any adjustments
to the mechanical ventilator. If the BE is more positive than +6 or the BD
is more negative than –6, metabolic alkalosis is likely present, although
it is uncommon during donor care.
Treatment
• Metabolic acidosis: If the arterial pH remains below 7.32 after following
the recommended changes in the mechanical ventilation guideline
(section IVA), administer a slow intravenous push of a pre-mixed
syringe of sodium bicarbonate (NaHCO
3
) with a concentration of 44 or
50 mEq. However, if the sodium level is concurrently above 150 mEq/L,
consult a physician/intensivist before administering NaHCO
3
. If the
arterial pH remains below 7.32 after re-testing in 30 minutes, repeat the
administration of NaHCO
3
. If the arterial pH continues to remain below
7.32 thereafter, consult a physician/intensivist.
• Metabolic alkalosis: If the arterial pH remains above 7.45 after
implementing the recommended changes in the mechanical ventilation
guideline, consult an intensivist.
Note: Please consider these as guidelines only. It is advisable to refer to more current and advanced
medical literature for the most up-to-date information.
Medical Issues and Management
89
Dr Gopi Ayyaswamy
Donor Care Flow Sheet
Initial Problem List: New Problems:
Time
Heart rate
Blood pressure (Sys/Dias)
Mean arterial pressure (MAP)
Temperature
Urine output
ABG pH
PaCO
2
PaO
2
HCO
3
Sodium (Na)
Potassium (K)
Magnesium (Mg)
Calcium (Ca)
Phosphorus (P)
Capillary blood glucose (CBG)
Haematocrit (Hct)
WBC
Platelets
Prothrombin time (PT)
Partial thromboplastin time (PTT)
Fibrinogen
Medicines and uids
DOPA µ/k/min
Norepinephrine
Desmopressin (DDAVP
®
)
Normal saline 0.9%
Albumin (human) 5%
Others
Dr Gopi Ayyaswamy
Complexities of Intensive Care
12
Organ donation and transplantation represent profound milestones in the
realm of modern medicine. This progress is rooted in centuries of dreams,
the relentless pursuit of knowledge, and remarkable technical innovations.
At its core, organ donation is a seless act that not only holds the power to
save more than ve lives but also has the potential to dramatically enhance
the quality of life for countless others through tissue donation.
However, within the domain of intensive care, particularly when
dealing with brain-dead individuals in the context of organ donation and
transplantation, the intensivist encounter a complex and multifaceted
landscape. It is here that the true intricacies of this medical marvel come to
light. The responsibility to navigate these intricacies falls upon the clinical
team, who must not only adhere to evidence-based best practices that
benet the recipient but also respect and honour the wishes of the donor’s
family. Achieving this delicate balance necessitates the standardization of
best practices while accounting for the unique circumstances and resources
of each medical institution.
When a patient suffers a severe brain injury, such as a traumatic
brain injury or a debilitating stroke, which leads to irreversible brain
stem dysfunction, a diagnosis of brain death may be pronounced. In
these challenging and emotionally charged cases, a patient’s previously
expressed wishes and the preferences of their family become crucial factors
in determining whether the patient can become a potential candidate for
organ and tissue donation. The decision to donate organs is a family-driven
process inuenced by a multitude of factors, including social, educational,
and spiritual considerations. In such trying moments, a representative from
92
A Simple Introduction to Organ Transplant
Dr Gopi Ayyaswamy
the transplant team preferably the counsellor or a specially trained hospital
staff member steps forward to engage in compassionate communication
with the grieving family. Their role is to guide the family through the
organ donor management process, offering support, information, and
reassurance during this emotionally fraught period.
Given the immense emotional sensitivity that surrounds the loss of a
loved one, it is paramount that healthcare professionals provide thoughtful
education and consider the needs and wishes of the family members. This
approach to organ donation hinges on a comprehensive understanding
of the medical procedures involved and the ethical considerations that
underscore the entire process.
Within the connes of a hospital’s neuro-intensive care unit, a central
concern revolves around the meticulous management of the brain-dead
individual, with a primary focus on optimizing the preservation and
subsequent transfer of donor organs. Once brain death is conrmed,
comprehensive medical care for the donor begins. This care may involve
the administration of appropriate medications to maintain basic bodily and
organ functions within physiological limits. The preservation of organs
becomes a critical objective before extraordinary support measures, such as
pharmacological interventions for hemodynamics and ventilator support
for respiration, can be gradually withdrawn.
To achieve this, vigilant monitoring and maintenance of physiological
parameters, including blood pressure, respiratory rate, and uid and
electrolyte balance, are essential. Medications such as corticosteroids and
thyroid hormones may be employed, alongside adjustments to ventilator
settings and uid administration, to sustain organ function and overall
stability. This orchestration requires a synchronized effort among the
clinical team, involving meticulous management of the brain-dead cadaver
and coordinated interactions with the patient’s family.
As medical professionals strive to uphold the donor’s wishes and
maximize the potential for successful organ transplantation, collaboration
is key. Each team member plays a vital role in ensuring that the implanted
organ functions optimally post-transplantation. This collaborative
approach not only involves the medical staff but also extends to the
family members, who must work harmoniously with transplant team
Complexities of Intensive Care
93
Dr Gopi Ayyaswamy
representatives. By doing so, the transplantation process becomes a symbol
of hope, offering new lease on life to recipients while honouring the seless
gift of life bestowed by organ donors and their families.
The world of organ donation and transplantation is a testament to
human resilience, compassion, and scientic achievement. It represents the
culmination of centuries of dreams, knowledge, and technical innovation.
However, it is within the walls of intensive care units that the most
intricate and profound challenges are faced. These challenges are met with
unwavering dedication from healthcare professionals who work tirelessly
to save lives and offer the gift of life to those in need. Organ donation is
not just a medical procedure; it is a testament to the power of humanity
to come together, make difcult decisions, and provide hope in the face
of adversity.
Unravelling the Complexities of Physiological Changes in Brain Death
Brain death is a pivotal event in the world of organ transplantation,
triggering a cascade of intricate physiological changes within the body.
These changes have a profound impact on the overall function and
stability of various organ systems. Understanding these physiological
transformations are paramount, as they signicantly inuence the success
of organ donation and transplantation, shedding light on the multifaceted
challenges faced in intensive care units.
One of the rst notable changes that occur following brain death is the
resolution of the sympathetic surge initially accompanying herniation.
Subsequently, there is a variable loss of sympathetic tone, leading to
vasodilation and reperfusion injury. These processes collectively contribute
to the development of various complications frequently observed in organ
donors, including hypotension, arrhythmias, endocrine deficiencies,
electrolyte imbalances, and hypothermia. These complications underscore
the critical need for vigilant management in intensive care settings.
The occurrence of brain death also triggers the depletion of the body’s
high-energy stores, setting the stage for a series of complex biochemical
events. As brain death progresses, there is an overwhelming inux of
calcium ions (Ca
2+
) into cells, disrupting the delicate balance maintained by
ionic pumps. This inux results in endothelial swelling and the accumulation