Transcript Endocrine dysfunction ICU management

SURGICAL
CONDITIONS
THYROIDECTOMY
ENDOCRINE DYSFUNCTION - MANAGEMENT
THYROIDECTOMY
TOTAL THYROIDECTOMY – THYROID
REPLACEMENT IS REQUIRED
SUBTOTAL THYROIDECTOMY – USE
SERUM THYROID LEVEL AS AN
INDICATOR
THYROIDECTOMY - MEDICATION
THYROXINE REPLACEMENT
HALF LIFE OF THYROXINE IS FEW DAYS,
THEREFORE CAN WAIT TILL STARTING
RX.
DOSE (L-THYROXINE) : 0.15 – 0.2mg dly
THYROIDECTOMY - MEDICATION
TSH
 USED AS SUPPRESSION FOR…
1)NON-TOXIC GOITER
2)OR IF SUBTOTAL THYROIDECTOMY
3)FOR TOTAL THYROIDECTOMY FOR
THYROID CA (SELECTED CASES)
 DOSE : 0.2 – 0.4mg dly
THYROIDECTOMY - MEDICATION
PROPANOLOL
IF PT WAS GIVEN PRE-OP
PROPANOLOL, ADVISABLE TO CONTINUE
2 -3 DAYS POST OP.
THYROIDECTOMY - MEDICATION
HYPOPARATHYROIDISM
Hypoparathyroidism can occur post
surgery.
More likely in extensive dissection for
diffuse nature or malignancy (esp. radical
neck dissection)
THYROIDECTOMY - MEDICATION
THYROID STORM
MX OVERVIEW
Can occur as a complication post
surgery.
Manage precipitating factors
Reduce synthesis and release of thryoid
hormones.
Reduce peripheral conversion of T4 to
T3.
THYROIDECTOMY – THYROID STORM
SUPPORTIVE MEASURES
These pts are hypermetabolic and need
more fluids electrolytes and glucose.
Bring down fever (but don’t use
salicylates – they diplace thyroid
hormones from their binding prots.)
Plasma exchange as last resort – not
proven to work
THYROIDECTOMY – THYROID STORM
B-ADRENERGIC BLOCKERS
FUNCTIONS
Antagonises the effect of thyroid
hormones.
Decreases the
hypersensitivity to
cathecholamines.
THYROIDECTOMY – THYROID STORM
B-ADRENERGIC BLOCKERS
PROPANOLOL
Drug of choice as it also inhibits
peripheral conversion of t4 to t3
It promptly treats the tachycardia, fever,
hyperkinesis & tremor
IV doses of 0.5mg with cardiac
monitoring up to 10mg
Give more 4-6 hrly
THYROIDECTOMY - THYROID STORM
B-ADRENERGIC BLOCKERS
OTHER AGENTS
B1 selective agents not as good – do not
inhibit T4 to T3
Use when Propanolol contra-indicated.
Esmolol 250-500micg/kg bolus followed
by 50-100mcg/kg/min.
(Diltiazam also good in reducing pulse
rate.)
THYROIDECTOMY - THYROID STORM
CORTICOSTEROIDS
Given because of the relative
deficiency.
Also used beacue they inhibit periph.
conversion T4 to T3.
Hydrocortisone 100mg ivi 6hrly or
Dexamethasone 5mg ivi 12 hrly
THYROIDECTOMY - THYROID STORM
THIONAMIDES
Propylthiouracil
No parental form avail. – and in thyrotox, GI absorp is down
Rapid onset
Function – blocks iodination of Tyrosine and inhib of periph.
Conversion (T4 – T3)
Dose: 100mg loading then 100mg 2 hrly
Methimazole
Slower onset, but longer action.
Does not inhibit periph. Conversion (T4-T3)
Dose: 100mg bolus then 20mg 8hrly
Carbimazole
It is metabolised to methimazole
For all…..
Transient leukopaenia
(20%). Agranulocytosis
is rare
THYROIDECTOMY - THYROID STORM
IODINE
In large doses, it inhibits synthesis and
release of thyroid hormones
Give 1 hr after thioamides
Preps are Lugol’s iodine(oral),
potassium iodide, sodium iodide
Dose: Sodium iodide 1g ivi 12hrly or
equiv oral doses
Iodine containing contrast media are
very good as they are more potent
inhibiters of periph conversion.
THYROIDECTOMY - THYROID STORM
LITHIUM CARBONATE
Used for patients allergic to iodine.
Similar action
Dose: 500-1500mg dly.
Drug monitoring of Lithium.
THYROIDECTOMY - THYROID STORM
DIGOXIN
Use if AF or heart failure present.
Larger than normal doses because of
the high BMR
THYROIDECTOMY - THYROID STORM
AMIODARONE
Controls Arrythmias
Inhibits peripheral conversion of T4 to
T3.
THYROIDECTOMY - THYROID STORM
THYROIDECTOMY – MORE COMPLICATIONS
MYXOEDEMA COMA
Thyroid hormones
T3 best idea.
Dose: 20mcg/d.
T4 not good because periph. conversion is decreased.
Steroids
Given because these pts have impaired glucocorticoid
response to stress., or co-existant adrenal insuff. (Schmidt’s
syndrome)
Dose: Hydrocortisone 200-300mg/d
Supportive
These pts have reduced response to hypoxia and hypercarbia, and
decreased GCS, so ventilation often required.
Warm to treat hypothermia
Rx hyponatraemia, hypoglycaemia
PARATHYROIDECTOMY
PARATHYROIDECTOMY
INTRO
Adenoma and hyperplasia. Removal of
multiple glands usually with hyperplasia.
Transient hypopara. after gland
removal.
Suppression of normal glands
If hypocalcaemia occurs within the first
12-18 hrs, then it is likely to be severe.
PARATHYROIDECTOMY
CALCIUM REPLACEMENT
Mild hypocalcaemia – just watch
Mild hypocal with tingling of lips,
fingers, toes – oral therapy.
Tetany – IVI Calcium
NB – pts on digitalis are more
susceptible to arrthmias
Vit D is usually withheld for 4 – 6 weeks,
unless it is difficult to maintain the Ca.
Parathyroids usually recover within this
period.
PARATHYROIDECTOMY
HYPOCALCAEMIA – GENERAL ASPECTS
Generally a problem in 70-90% of ICU
patients.
IVI calcium…
Two forms. Chloride and gluconate.
Diff. btw 2 is the amount of elemental ca
avail at equiv volumes
Avoid rapid admin – causes nausea, flushing, headache
arrythmias.
Dose – 100mg bolus, then 1-2mg/kg
If not coming up with IVI replacement – consider Mg
deficiency
Calcitrol is usually used for the more chronic conditions.
ADRENALECTOMY
ADRENALECTOMY
ADRENALECTOMY – INDICS.
Bilateral adrenalectomy most often
done for disseminated breast CA.
Old days, done for HPT. Now medical
mx is good enough
Hyperplastic states from pituitary
tumours
Neoplasms
ADRENALECTOMY
MANAGEMENT
Treat complications - bleeding,
pneumothorax, esp if 12th rib is resected.
Ileus following retroperitoneal
dissection.
Treat Adrenocortical Insufficiency…
ADRENALECTOMY
ADRENOCORTICAL INSUFFICIENCY
Be aggressive. Start even before blood
levels available.
Anticipate who will need –
Adrenalectomy, pt’s who are supressed
from steroid therapy, pt’s with adrenal or
pituatary disease.
Do not replace as a ‘standard’.
ADRENALECTOMY
ADRENOCORTICAL INSUFFICIENCY
Start replacement with induction of
anaesthesia.
Start with Dexamthasone 10mg IVI,
together with ACTH 0.25 ivi (synacthen)
Continue steroid replacement with
Hydrocortisone 100mgiv 6-8hrly. Taper.
Taper then to oral.
Hydrocortisone has sufficient
mineralocrticoid component.
ADRENALECTOMY
GENERAL MEASURES
Avoid opiates and sedatives
Correct electrolyte and glucose
Fluid balance
Ecg monitoring
Treat shock
Fluids need to be aggressive initially
PHAEOCHROMOCYTOMA
PHAEOCHROMOCYTOMA
GENERAL
Tumour of the Adrenal Medulla
No other surgical problems for
consideration in the adrenal medulla
PHAEOCHROMOCYTOMA
PROCEDURES DURING SURGERY
Prep for surgery: alpha-adrenergic
blocker as soon as dx made
Phenoxybenzamine 10-100mg b.d. for at
least 3 d before Sx.
Phentolamine (1-5mg) can be used for
immed effect if the BP rises during sx
Approp. inotropes and volume
expanders to be used if BP drops after
removal.
 Propanolol can be used pre, intra, and
post op to prevent and Rx cardiac
arrythmias. Oral or IVI (10th the oral
dose).
PHAEOCHROMOCYTOMA
POST SURGERY
Few days post Sx: urinary
Vanillymandelic Acid and
Cathecholamines to verify proper
removal of tumour.
If bilateral adrenalectomy was done –
consider corticosteroid replacement.
PITUITARY
SURGERY
PITUATARY SURGERY
INTRO
ACTH replacement must be given as
described
Remember, with pharmacologic doses
of steroids, underlying diabetes may be
unmasked, and DKA etc must be
managed.
PITUATARY SURGERY
ADH DEFICIENCY
This occurs unless the stalk is left
intact, there may be no deficiency.
 Triphasic response to sx….
1)Immed post sx – polyuria and polydipsia
– 4 to 5 days
2)Intense anti-diuresis for 6 days
3)Permanent poyuria and polydipsia (DI)
 Phase one is due to damage to hypothalamus tissue and
hormone not released.
 Phase 2 is due to degeneration of hormone laden stores.
Fluid admin during this phase will not induce the usual
diuretic response.
PITUATARY SURGERY
ADH DEFICIENCY
MANAGEMENT
 During polyuric phase – watch fluid
balance and electrolytes carefully.
 Rx with ADH to decrease urine to
normal values, withan increasein
specific gravity.
 DDAVP is treatmentrx of choice.
NON-SURGICAL
ISSUES
NON-SURGICAL ISSUES
HYPERGLYCAEMIA
INTRO
Hyperglycemia is a common metabolic
feature of severe stress and is becoming
recognized as a harbinger of the severity
and outcome of illness.
The effects of counterregulatory
hormones and pro-inflammatory
cytokines predominate as a cause
Reversing hyperglycemia and insulin
resistance reduces mortality
NON-SURGICAL ISSUES
HYPERGLYCAEMIA
INTRO - CONTINUED
Trials have shown that aggressive
treatment of hyperglycemia has a positive
impact on immune recovery and the recovery
from an MI
One study: Mortality was decreased by 34%
in a surgical ICU by “clamping” the glucose
level between 4.4 and 6.1 mmol/L
Insulin may have anti-inflammatory
properties – but achieving normoglycaemia
more important than insulin dose.
NON-SURGICAL ISSUES
HYPERGLYCAEMIA
INTRO - CONTINUED
BBA’s relieve Stress Hyperglycaemia, thus
implicating cathecholamines to the disorder.
Metformin particularly useful in SH. It
has antihyperglycemic effects via
suppression of glucose production of the
liver as well as having antioxidant
properties – but beware lactic acidosis
GROWTH
HORMONE
NON-SURGICAL ISSUES
GROWTH HORMONE
INTRO
Despite aggressive nutritional support,
critically ill patients remain catabolic
with continued nitrogen loss.
GH supplementation has salutary
anabolic effects in stressful conditions,
but is poven to increase risk of mortality
GH replacement: If GH low, can be
replaced with recombinant GH- appears
safe
NON-SURGICAL ISSUES
GROWTH HORMONE
DELITARIOUS EFFECTS
Oedema
Insulin resistance
Exacerbated microvascular injury in the
face of sepsis
Hyperglycaemia
Induces hepatic enzymes
HPA
INSUFFICIENCY
HPA INSUFFICIENCY
INTRO
Adrenal insufficency occurs in 20% of
ICU pts
Induced by sepsis, hypovolaemia,
stress, drugs
Both high and low cortisol levels assoc.
with poor prognosis.
Higher levels assoc. with higher
APACHE and SOFA scores = poorer
prognosis
HPA INSUFFICIENCY
EXAMPLES
Cortisol > 1200 nmol/l in sepsis and resp
failure.
Cortisol > 745 nmol/l in ruptured AAA.
A ‘normal’ level for ICU patients cannot
be defined.
Use Synacthen and ACTH test.
HPA INSUFFICIENCY
CORTISOL SUPPLEMENTATION
Physiological doses of glucocorticoids
of 300 mg per day leads to
supraphysiological circulating cortisol
levels
In a multicentre trial, septic pts given
high dose cortisol – higher death rate
than placebo group.
HPA INSUFFICIENCY
CORTISOL SUPPLEMENTATION
Concept of “relative adrenal
insufficiency” and “low-dose” (ie, 100 to
300 mg per day) corticosteroid therapy.
Initial trials showed promising trends in
subgroups of patients with sepsis.
The beneficial effects were restricted to
improvements in hemodynamics and a
reduction in the need for vasopressor
therapy.
HPA INSUFFICIENCY
GENERAL CONCEPTS
The beneficial effect of steroids
remains unproven, and a conservative
approach is more prudent.
Clinician must rely on a clinical
assessment of the severity of the stress,
(evaluate misleading symptoms) to
estimate the adequacy of the measured
cortisol.
Clues of adrenal dysfunction, such as
unexplained eosinophilia
HPA INSUFFICIENCY
GENERAL CONCEPTS
Certain conditions - TB, Meningitis, Typhoid
fever, and PCP - the use of glucocorticoids
appears less controversial
Can be considered in selected highriskpatients, predominantly in septic shock
patients, while awaiting confirmatory results
of HPA testing.
Steroid therapy should be stopped if results
of HPA testing become available and do not
indicate the presence of adrenal
insufficiency
THE
END