Acromegaly

D E FI N I T ION 

Constellation of signs and symptoms caused by hypersecretion of GH in

adults. (Excess GH before puberty results in gigantism.)

AE T IOLOGY 

Most cases are a result of GH-secreting pituitary adenoma.

Rarely: Excess GHRH causing somatotroph hyperplasia from hypothalamic ganglioneuroma,

bronchial carcinoid or pancreatic tumours.

E P IDEMIOLOGY 

Rare. Annual incidence of five in 1 000 000. Age at diagnosis: 40–50

years.

H ISTORY 

Very gradual progression of symptoms over many years (often only detectable on

serial photographs).

May complain of rings and shoes becoming tight.

" Sweating, headache, carpal tunnel syndrome.

Symptoms of hypopituitarism (hypogonadism, hypothyroidism, hypoadrenalism). Visual

disturbances (caused by optic chiasm compression).

Hyperprolactinaemia (irregular periods, # libido, impotence).

EXAMINA T I ON

 Hands: Enlarged spade-like hands with thick greasy skin. Signs of carpal

tunnel syndrome (see Carpal tunnel syndrome). Pre-mature osteoarthritis (arthritis also

affects other large joints, temporomandibular joint).

Face: Prominent eyebrow ridge (frontal bossing) and cheeks, broad nose bridge, prominent

nasolabial folds, thick lips, " gap between teeth, large tongue, prognathism, husky

resonant voice (thickening vocal cords).

Visual field loss: Bitemporal superior quadrantanopia progressing to bitemporal hemianopia

(caused by pituitary tumour compressing the optic chiasm).

Neck: Multi-nodular goitre.

Feet: Enlarged.

INVE S T I G A T IONS

 Serum IGF-1: Useful screening test. GH stimulates liver IGF-1 secretion

(IGF-1 varies with age of patient and " during pregnancy and puberty).

Oral glucose tolerance test: Failure of suppression of GH after 75 g oral glucose load (falsepositive

results are seen in anorexia nervosa, Wilson’s disease, opiate addiction).

Pituitary function tests: 9 a.m. cortisol, free T4 and TSH, LH, FSH, testosterone (in men) and

prolactin (to test for hypopituitarism).

MRI of the brain: To image the pituitary tumour and effect on the optic chiasm.

MANAGEMENT 

Surgical: Trans-sphenoidal hypophysectomy is the only curative

treatment.

Radiotherapy: Adjunctive treatment to surgery.

Medical: If surgery is contra-indicated or refused.

SC somatostatin analogues (octreotide, lanreotide). Side-effects: abdominal pain, steatorrhoea

glucose intolerance, gallstones, irritation at the injection site.

Oral dopamine agonists (bromocriptine, cabergoline). Side-effects: nausea, vomiting, constipation,

posturalhypotension ("dose graduallyandtake it during meals), psychosis (rare).

GH antagonist (pegvisomant)

Monitor: GH and IGF1 levels can be used to monitor disease control. Pituitary function tests,

echocardiography, regular colonoscopy and blood glucose.

COM P L IC A T I ONS 

CVS: Cardiomyopathy, hypertension.

Respiratory: Obstructive sleep apnoea.

Gl: Colonic polyps.

Reproductive: Hyperprolactinaemia (30%).

Metabolic: Hypercalcaemia, hyperphosphataemia, renal stones, diabetes mellitus,

hypertriglyceridaemia.

ENDOCRINOLOGY 

193

Acromegaly (continued)

Psychological: Depression, psychosis (resulting from dopamine agonist therapy).

Complications of surgery: Nasoseptal perforation, hypopituitarism, adenoma recurrence, CSF

leak, infection (meninges, sphenoid sinus).

P ROGNOS I S 

Good with early diagnosis and treatment, although physical changes are

irreversible.

2 تعليق

PH.Jafar Jassim 11/27/2020 11:58:00 م

تابع القراءه

Adrenal insufficiency

D E FI N I T ION

 Deficiency of adrenal cortical hormones (e.g. mineralocorticoids, glucocorticoids

and androgens).

AE T IOLOGY

 Primary (Addison’s disease): Autoimmune (>70%).

Infections: Tuberculosis, meningococcal septicaemia (Waterhouse–Friderichsen syndrome),

CMV (HIV patients), histoplasmosis.

Infiltration: Metastasis (e.g. lung, breast, melanoma), lymphomas, amyloidosis.

Infarction: Secondary to thrombophilia

Inherited: Adrenoleukodystrophy1, ACTH receptor mutation.

Surgical: After bilateral adrenalectomy.

Secondary: Pituitary or hypothalamic disease.

Iatrogenic: Sudden cessation of long-term steroid therapy.

E P IDEMIOLOGY

 Most common cause is iatrogenic. Primary causes are rare (annual

incidence of Addison’s is eight in 1 000 000).

H ISTORY 

Chronic presentation: Non-specific vague symptoms such as dizziness, anorexia,

weight loss, diarrhoea, vomiting, abdominal pain, lethargy, weakness, depression.

Acute presentation (Addisonian crisis): Acute adrenal insufficiency with major haemodynamic

collapse often precipitated by stress (e.g. infection or surgery).

EXAMINA T I ON

 Postural hypotension.

Increased pigmentation: Generalized but more noticeable on buccal mucosa, scars, skin

creases, nails, pressure points (resulting from melanocytes being stimulated by " ACTH

levels).

Loss of body hair in women (androgen deficiency).

Associated autoimmune conditions: e.g. vitiligo.

Addisonian crisis: Hypotensive shock, tachycardia, pale, cold, clammy, oliguria.

INVE S T I G A T IONS 

Confirm the diagnosis: 9 a.m. serum cortisol < 100 nmol/L is diagnostic

of adrenal insufficiency. If 9 a.m. cortisol > 550 nmol/L: adrenal insufficiency is unlikely.

Patients with 9 a.m. cortisol of between 100 and 550 nmol/L should have a short ACTH

stimulation test (short Synacthen test): IM 250 mg tetracosactrin (synthetic ACTH) is given.

Serum cortisol <550 nmol/L at 30 min indicates adrenal failure.

Identify the level of defect ACTH: " in primary disease and # in secondary disease. Long

Synacthen test: One milligram tetracosactrin is given and cortisol is measured at 0, 30, 60,

90 and 120 min then at 4, 6, 8, 12 and 24 h. Patients with primary adrenal insufficiency

show no increase after 6.

Identify the cause: Autoantibodies (against 21-hydroxylase). Abdominal CT or MRI. Other

tests e.g. adrenal biopsy for microscopy, culture, PCR depending on the suspected

causes.

Check TFTs

Investigations in ‘Addisonian crisis’: FBC (neutrophilia), U&E (" urea, # Naþ, " Kþ), ESR or

CRP (" in acute infection), Ca2þ

(may be "), glucose (#), blood cultures, urinalysis, culture

and sensitivity (UTI may have triggered the crisis). CXR: May identify cause (e.g.

tuberculosis, carcinoma) or precipitant of crisis (e.g. infection).

MANAGEMENT

 Addisonian crisis: Rapid IV fluid rehydration (0.9% saline, 1 L over

30–60 min, 2–4 L in 12–24 h).50ml of 50%dextrose to correct hypoglycaemia. IV 200mg

hydrocortisone bolus followedby 100mg6 hourly (until BP is stable). Treat the precipitating

cause (e.g. antibiotics for infection).Monitortemperature, pulse, respiratory rate, BP, satO2

and urine output.

1Adrenoleukodystrophy is an X-linked inherited disease characterized by adrenal atrophy and

demyelination

Adrenal insufficiency (continued)

Chronic: Replacement of glucocorticoids with hydrocortisone (three times/day) and mineralocorticoids

with fludrocortisone. Hydrocortisone dosage needs to be increased during

acute illness or stress. If associated with hypothyroidism, give hydrocortisone before

thyroxine (to avoid precipitating an Addisonian crisis).

Advice: Steroid warning card, Medic-alert bracelet, emergency hydrocortisone ampoule,

patient education.

COMPL I C A T IONS 

Hyperkalaemia. Death during an Addisonian crisis.

P ROGNOS I S

 Adrenal function rarely recovers, but normal life expectancy can be expected

if treated.

Type I (autosomal recessive disorder caused by mutations in the AIRE gene which encodes a

nuclear transcription factor.): Addison’s disease, chronic mucocutaneous candidiasis,

hypoparathyroidism.

Type II (Schmidt’s syndrome): Addison’s disease, diabetes mellitus Type 1, hypothyroidism,

hypogonadism.

†

2 تعليق

PH.Jafar Jassim 11/15/2020 11:28:00 م

تابع القراءه

Carcinoid syndrome

D E FI N I T ION 

Constellation of symptoms caused by systemic release of humoral factors

(biogenic amines, polypeptides, prostaglandins) from carcinoid tumours.

AETIOLOGY 

Carcinoid tumours are slow-growing neuroendocrine tumours mostly derived

from serotonin-producing enterochromaffin cells. They produce secretory products

such as serotonin, histamine, tachykinins, kallikrein and prostaglandin. May be classified into

fore-, mid- or hindgut tumours. 75–80%of patients with the carcinoid syndrome have small

bowel carcinoids. Common sites for carcinoid tumours include appendix and rectum, where

they are often benign and non-secretory. Also found in other parts of large intestine,

stomach, thymus, bronchus and other organs. Hormones released into the portal circulation

are metabolized in the liver. Thus symptoms typically do not appear until there are hepatic

metastases (resulting in the secretion of tumour products into the hepatic veins), or release

into the systemic circulation from bronchial or extensive retroperitoneal tumours.

E P IDEMIOLOGY

 Rare, annual UK incidence is one in 1 000 000. Asymptomatic carcinoid

tumours are more common and may be an incidental finding after rectal biopsy or

appendectomy. Ten percent of patients with multiple endocrine neoplasia (MEN) type 1

have carcinoid tumours.

H ISTORY

 Paroxysmal flushing, diarrhoea, crampy abdominal pain, wheeze, sweating,

palpitations.

EXAMINA T I ON

 Facial flushing, telangiectasia, wheeze.

Right-sided heart murmurs: Tricuspid stenosis, regurgitation or pulmonary stenosis.

Nodular hepatomegaly in cases of metastatic disease.

Carcinoid crisis: Profound flushing, bronchospasm, tachycardia and fluctuating blood

pressure.

INVE S T I G A T IONS 

24-h urine collection: 5-HIAA levels (a metabolite of serotonin, false

positive with high intake of certain fruit/drugs e.g. bananas and avocados, caffeine,

paracetamol).

Blood: Plasma chromogranin A and B, fasting gut hormones.

CT or MRI scan: To localizes the tumour.

Radioisotope scan: Radiolabelled somatostatin analogue (e.g. indium-111 octreotide) helps

localize tumour.

Investigations for MEN-1: (see footnote to Hyperparathyroidism).

MANAGEMENT 

Carcinoid crisis: Octreotide infusion, also IV antihistamine and

hydrocortisone.

Multidisciplinary approach (endocrinologists/gastroenterologists, oncologists, radiologists

and surgeons).

Advice: Avoid precipitating factors e.g. alcohol, strenuous exercise.

Somatostatin analogues (e.g. octreotide) inhibit hormone release and tumour growth.

Radiolabelled octreotide may be beneficial (receptor-targeted therapy).

Interferon-a: May be given on its own or added to long-acting somatostatin analogues if the

patient is not responding to the maximum dosage of somatostatin analogues.

Supportive: Ondansetron and cyproheptadine (5-HT antagonists) can alleviate symptoms,

rehydration (for diarrhoea), antiemetics and anti-diarrhoeal treatment (codeine,

loperamide).

Surgery: Should be considered for resectable nodal or hepatic metastasis, extraintestinal

(bronchial and ovarian) carcinoids. Small intestinal carcinoids may be resected even in the

presence of metastases, to prevent fibrosing mesenteritis. Valve surgery for symptomatic

carcinoid heart disease. A potential peri-operative carcinoid crisis should be prevented by

prophylactic treatment with octreotide

Carcinoid syndrome (continued)

Hepatic artery embolization: For patients with non-resectable multiple and hormone secreting

tumours. Two types: particle and chemoembolization.

COMPL I C A T IONS

 Electrolyte imbalance (secondary to diarrhoea), metastases, bowel

obstruction (due to fibrosis near a gut primary), tricuspid and pulmonary valve stenosis with

consequent right heart failure, pellagra: dermatitis, glossitis, diarrhoea, dementia (due to

niacin deficiency caused by diversion of dietary tryptophan for the synthesis of large amounts

of serotonin).

P ROGNOS I S

 Median survival is usually 5–10 years but can range up to 20 years.

Earlier detection and treatment should improve quality of life and survival.

6 تعليق

PH.Jafar Jassim 11/09/2020 11:09:00 م

تابع القراءه

Congenital adrenal hyperplasia

D E FI N I T ION

 Inherited disorders of adrenal steroid synthesis.

AE T IOLOGY 

Autosomal recessive genetic defects in the steroid synthesis pathway result in

# cortisol (and, in some cases, # aldosterone) synthesis. This produces a secondary rise in

pituitary ACTH secretion causing hyperplasia of the adrenal glands and build-up of precursor

steroids and in most cases androgenic steroids. Common defective enzymes include 21-

hydroxylase (most common), 11b-hydroxylase and 17a-hydroxylase.

E P IDEMIOLOGY 

Annual incidence of 21-hydroxylase deficiency and 11b -hydroxylase

deficiency are one in 10 000 and one in 100 000, respectively. The rest are less common.

H ISTORY AND EXAMI N AT ION 

21-Hydroxylase deficiency (# aldosterone, " androgens):

Classic: Salt-losing crisis in infants (hypotension, hyponatraemia, hyperkalaemia). Females:

Ambiguous genitalia (cliteromegaly, fused labia). Males: Precocious puberty.

Non-classic or late-onset CAH: Hirsutism, acne and menstrual irregularity in young women,

early pubarche or sexual precocity in school age children, or there may be no symptoms.

11 b-Hydroxylase deficiency ("11-deoxycorticosterone: a mineralocorticoid, " androgens):

Hypertension, hypokalaemia.

Females: Ambiguous genitalia. Males: Precocious puberty.

17a-Hydroxylase deficiency (" aldosterone, # androgens): Hypertension, hypokalaemia.

Females: Failure to develop secondary sexual characteristics at puberty. Males: Ambiguous

genitalia.

INVE S T I G A T IONS

 Blood: 9 a.m. follicular phase 17OH-progesterone (" in 21-hydroxylase

deficiency and 11b-hydroxylase deficiency), testosterone, LH, FSH, U&Es. ACTH stimulation

test: Inappropriately elevated 17OH-progesterone levels after IM synthetic ACTH. Karyotyping:

Confirms gender of infantwith ambiguous genitalia. Genetic analysis may be performed

to identify specific CYP21 mutations. Men who desire future fertility: Serum testosterone

level, semen analysis and testicular ultrasound.

MANAGEMENT 

Acute salt-losing crisis: IV saline, dextrose and hydrocortisone.

Glucocorticoid replacement with dexamethasone or hydrocortisone. Fludrocortisone in saltlosers.

Monitor growth in children, serum 17OH-progesterone, DHEAS, androstenedione and

testosterone (goal: slightly above the normal range). Monitor plasma renin activity and

U&Es in patients on mineralocorticoids.

Children with ambiguous genitalia: Careful evaluation by an experienced team of paediatric

endocrinologists, geneticists and paediatric surgeons (reconstructive surgery at age 2–6

months). Psychosocial support.

Non-classic CAH: If not pursuing fertility, oral contraceptives or cyproterone acetate (antiandrogen).

Those who desire fertility should receive glucocorticoids; if do not ovulate add

clomiphene citrate. Males do not usually require treatment unless they have testicular

masses (see Complications) or oligospermia (in a man desiring fertility).

CAH and pregnancy: The male partner must be screened for CAH. If 17OH-progesterone

levels are elevated, genotyping must be done. If the male partner is heterozygote, then

the foetus is at risk of inheriting CAH and developing virilization. Thus pre-natal

dexamethasone is given to the mother as soon as the pregnancy is recognized.

COM P L IC A T I ONS 

Reduced fertility (caused by hyperandrogenaemia due to inadequate

glucocorticoid therapy or structural abnormalities due to androgen excess in utero or

suboptimal surgical reconstruction). Short final adult height (because of pre-mature epiphyseal

closure). Testicular adrenal rests (ectopic adrenal tissue which is stimulated by the

increased ACTH).

PROGNOSIS

 Undiagnosed infants may die from salt-losing crisis. Otherwise, quality of life

is usually good

5 تعليق

PH.Jafar Jassim 11/03/2020 11:25:00 م

تابع القراءه

Cushing‘s syndrome

D E F I N I T I ON 

Syndrome associatedwith chronic inappropriate elevation of free circulating

cortisol.

AET IOLOGY

 ACTH-dependent (80%)

. Excess ACTH secreted from a pituitary adenoma: Cushing’s disease (80%).

. ACTH secreted from an ectopic source, e.g. small-cell lung carcinomas, pulmonary

carcinoid tumours (20%).

ACTH-independent (20%)

. Excess cortisol secreted from a benign adrenal adenoma (60%).

. Excess cortisol secreted from an adrenal carcinoma (40%).

Rare: ACTH-independent micro- or macronodular adrenal hyperplasia1.

E P IDEMI OLOGY 

Incidence reported as 2–4/1000000 per year, but may be more

common. Endogenous Cushing’s syndrome is more common in females. Peak incidence

is 20–40 years.

H ISTORY

 Increasing weight and fatigue. Muscle weakness, myalgia, thin skin, easy

bruising, poor wound healing, fractures (resulting from osteoporosis).

Hirsutism, acne, frontal balding. Oligo- or amenorrhoea, depression or psychosis.

EXAMI N A T ION

Facial fullness, facial plethora, interscapular fat pad.

Proximal muscle weakness, thin skin, bruises.

Central obesity, pink/purple striae on abdomen, breast, thighs.

Kyphosis (due to vertebral fracture). Poorly healing wounds.

Hirsutism, acne, frontal balding.

Hypertension. Ankle oedema (salt and water retention as a result of mineralocorticoid effect

of excess cortisol).

Pigmentation in ACTH-dependent cases.

(Signs in italic are more discriminatory)

I N V E S T IGATIONS

 Must only be performed in patients with a high pre-test probability.

Blood: Non-specific changes include hypokalaemia (particularly in ectopic Cushing’s), "

glucose.

Initial high-sensitivity tests:

Urinary free cortisol (two or three 24 h urine collections). Late-night salivary cortisol. Overnight

dexamethasone suppression test. Low dose dexamethasone suppression test (LDDST).

LDDST involves giving 0.5mg dexamethasone orally every 6 h for 48 h. In Cushing’s

syndrome, serum cortisol measured 48 h after the first dose of dexamethasone fails to

suppress below 50nmol/L.

Tests to determine the underlying cause:

ACTH-independent (adrenal adenoma/carcinoma): # Plasma ACTH. CT or MRI of adrenals.

ACTH-dependent (pituitary adenoma): " Plasma ACTH. Pituitary MRI. High-dose dexamethasone

suppression test (largely abandoned in centres where inferior petrosal sinus

sampling is available). Inferior petrosal sinus sampling: Central: peripheral ratio of venous

ACTH > 2:1 (or >3:1 after CRH administration) in Cushing’s disease.

ACTH-dependent (ectopic):

If lung cancer is suspected: CXR, sputum cytology, bronchoscopy, CT scan. Radiolabelled

octreotide scans to detect carcinoid tumours as they express somatostatin receptors.

MANAGEMENT 

In iatrogenic cases, discontinue administration, lower steroid dose or use

an alternative steroid-sparing agent if possible.

Medical: Pre-operative or if unfit for surgery. Inhibition of cortisol synthesis with metyrapone

or ketoconazole. Treat osteoporosis and provide physiotherapy for muscle weakness.

Surgical:

Pituitary adenomas: Trans-sphenoidal adenoma resection (hydrocortisone replaced until

pituitary function recovers).

Adrenal adenoma/carcinoma: Surgical removal of tumour (plus adjuvant therapy with

mitotane for adrenal carcinoma).

Ectopic ACTH production: Treatment is directed at the tumour.

Radiotherapy: In those who are not cured and have persistent hypercortisolaemia after transsphenoidal

resection of the tumour. Stereotactic radiotherapy provides less irradiation to

surrounding tissues.

In refractory cases of Cushing’s disease, bilateral adrenalectomy may be performed.

COM P L IC A T I ONS

 Diabetes, osteoporosis, hypertension. Pre-disposition to infections.

Complications of surgery: CSF leakage, meningitis, sphenoid sinusitis, hypopituitarism.

Complications of radiotherapy: Hypopituitarism, radionecrosis, small " risk of second

intracranial tumours and stroke.

Bilateral adrenalectomy may rarely be complicated by development of Nelson’s syndrome

(locally aggressive pituitary tumour causing skin pigmentation due to excessive ACTH

secretion).

PROGNOSIS 

In the untreated, 5-year survival rate is 50%. Depression usually persists for

many years following successful treatment.

1 Micronodular adrenal hyperplasia may be isolated or occur as part of Carney’s complex (autosomal

dominant syndrome characterized by spotty skin pigmentation, endocrine tumours and myxomas of the

skin, heart, breast). Three responsible genes have so far been identified: PRKAR1A, PDE11A, and MYH8.

Macronodular adrenal hyperplasia: Ectopic adrenal expression of G protein coupled receptors or "

expression/activity of some eutopic receptors. McCune–Albright syndrome is a rare variant caused by

activating mutations of the a-subunit of stimulatory G protein. It is characterized by caf
e au lait spots,

polyostotic fibrous dysplasia, precocious puberty and other endocrine disorders. Surgical bilateral adrenalectomy

is used in patients with micronodular adrenal hyperplasia and most patients with macronodular

adrenal hyperplasia.

ENDOCRINOLOGY

2 تعليق

PH.Jafar Jassim 11/01/2020 10:21:00 م

تابع القراءه

Diabetes mellitus, Type 1

D E F I N I T I ON Metabolic hyperglycaemic condition caused by absolute insufficiency of

pancreatic insulin production.

AET IOLOGY Caused by destruction of the pancreatic insulin-producing b-cells, resulting in

absolute insulin deficiency. The b -cell destruction is caused by an autoimmune process in

90% of patients.

Likely to occur in genetically susceptible subjects and is probably triggered by environmental

agents. Polymorphisms of a number of genes may influence the risk of type 1 diabetes.

These include the gene encoding preproinsulin and a number of genes related to immune

system function such as HLA-DQb and HLA-DR, PTPN22 and CTLA-4.

Pancreatic b-cell autoantigens may play a role in the initiation or progression of autoimmune

islet injury. These include glutamic acid decarboxylase (GAD), insulin, insulinoma-associated

protein 2 (IA-2) and cation efflux zinc transporter (ZnT8).

E P IDEMI OLOGY One of the most common chronic diseases in childhood with a prevalence

of 0.25% in the UK. Considerable geographic variation in the incidence. The US and

Northern Europe have an incidence of 8–17/100 000 per year.

H I S T O RY AND EXAMI N AT ION Often of juvenile onset (<30 years). Polyuria/nocturia

(osmotic diuresis caused by glycosuria), polydipsia (thirst), tiredness, weight loss. Symptoms

of complications (see below) Diabetic ketoacidosis: Nausea, vomiting, abdominal

pain, polyuria, polydipsia, drowsiness, confusion, coma, Kussmaul breathing (deep and

rapid), ketotic breath, signs of dehydration (e.g. dry mucous membranes, # tissue turgor).

Signs of complications: Fundoscopy (to look for diabetic retinopathy). Examination of feet

(test for neuropathy: 10 g monofilament testing and vibration sensation; palpate dorsalis

pedis and posterior tibial pulses). Measure BP.

Signs of associated autoimmune conditions e.g. vitiligo, Addison’s disease, autoimmune

thyroid disease.

I N V E S T IGATIONS Blood glucose: Fasting blood glucose >7 mmol/L or random blood

glucose >11 mmol/L. Two positive results are needed before diagnosis.

HbA1C: Estimates overall blood glucose levels in past 2–3 months.

FBC: MCV, reticulocytes (" erythrocyte turnover causes misleading HbA1c levels).

U&E: Monitor for nephropathy and hyperkalaemia caused by ACE inhibitors.

Lipid profile.

Urine albumin creatinine ratio (to detect microalbuminuria).

Patients presenting with suspected DKA Blood: FBC (" WCC even without infection), U&E ("

urea and creatinine from dehydration), LFT, CRP, glucose, amylase (may "), blood

cultures, ABG (metabolic acidosis with high anion gap), blood/urinary ketones.

Urine: Glycosuria, " ketones, MSU (microscopy, culture).

CXR: To exclude any infection.

ECG: To look for acute ischaemic changes.

MANAGEMENT Diabetic ketoacidosis Consider HDU/ICU input, central line, arterial line

and urinary catheter if severe acidosis, hypotensive or oliguric.

Insulin: 50U of soluble insulin in 50 mL 0.9% saline—start at 0.1 U/kg/h (6–7 U/h) until

capillary ketones <0.3, venous pH >7.30, and venous bicarbonate >18 mmol/L. At this

point, if the patient is able to eat and drink, change to SC insulin regimen. If not, change to

IV insulin sliding scale. Do not stop insulin infusion until 1–2 h after regular SC insulin is

restarted.

Fluids: 500mL 0.9%saline over 15–30 min until systolic BP >100mmHg. Then 1 L 2-hourly3

and 1 L 3-hourly3. IV dextrose is started in conjunction with 0.9% saline when blood

glucose reaches 15mmol/L: 1 L 5% dextrose over 8 h when blood glucose is 7–15mmol/L

and 500mL 10% dextrose over 4 h when blood glucose is <7mmol/L

Potassium replacement (start in the second bag of fluid, if passing urine). Adjust amount of

potassium added to fluids according to plasma potassium (If >5.50 mmol/L: Nil. If

2.5–5.5 mmol/L: 40 mmol/L, If <2.5 mmol/L 60–80 mmol/L).

Monitor blood glucose, capillary ketones and urine output hourly, U&Es 4-hourly, and venous

blood gas at 0, 2, 4, 8, 12 h and before stopping fixed rate insulin regimen. Monitor

phosphate and magnesium daily.

Broad spectrum antibiotics if infection suspected.

Thromboprophylaxis.

NBM for at least 6 h (gastroparesis is common).

NG tube: If GCS is reduced (to prevent vomiting and aspiration).

There is no strong evidence for the use of IV bicarbonate.

Refer to diabetes team for patient education.

Glycaemic control

Advice and patient education: Diabetes nurse specialists and dietitians. SC insulin: Shortacting

insulin (e.g. Lispro, aspart, glulisine) three times daily before each meal and one

long-acting insulin (isophane, glargine, detemir) injection once daily. Injection sites should

be rotated.

Insulin pumps may give slightly better glycaemic control. However, they are costly and

cumbersome for some patients and ketoacidosis may occur if the pump malfunctions.

Motivated patients can attend DAFNE (dose adjustment for normal eating) courses to learn

how to calculate their carbohydrate intake and adjust their insulin doses accordingly.

Monitor: Control of symptoms (e.g. thirst, tiredness), regular finger prick tests by the patient,

monitoring HbA1c levels (target <7%) every 3–6 months.1

Screening and management of complications. See Diabetes mellitus, Type 2.

Treatment of hypoglycaemia: If # consciousness: 50 ml of 50% glucose IV or 1mg glucagon

IM. If conscious and cooperative: 50 g oral glucose (e.g. in the form of Lucozade, milk,

sugar or 3 dextrose tablets), followed with a starchy snack. Should not drive for 45 min.

Screening and management cardiovascular risk factors See Diabetes mellitus, Type 2.

COM P L IC A T I ONS Diabetic ketoacidosis: # Insulin and " counter-regulatory hormones

result in " hepatic gluconeogenesis and # peripheral glucose utilization. Renal reabsorptive

capacity of glucose is exceeded causing glycosuria, osmotic diuresis and dehydration.

" Lipolysis leads to ketogenesis and metabolic acidosis. Diabetic ketoacidosis may be

precipitated by infection (30%), errors in management (15%), newly diagnosed diabetes

(10%), other medical disease (5%), no cause identified (40%).

Microvascular: Retinopathy, nephropathy, neuropathy (see Diabetes mellitus, Type 2).

Macrovascular: Peripheral vascular disease, ischaemic heart disease, stroke/TIA. Susceptible

to infections (especially on feet).Complications of insulin treatment: Weight gain. Fat

hypertrophy at insulin injection sites. Hypoglycaemia caused my missing a meal or

overdosage of insulin (Patients present with neuroglycopenic and adrenergic signs:

personality change, fits, confusion, coma, pallor, sweating, tremor, tachycardia, palpitations,

dizziness, hunger and focal neurological symptoms). Hypoglycaemic symptoms

may be masked by autonomic neuropathy, b-blockers and brain adapting to recurrent

episodes.

PROGNOSIS Depends on early diagnosis, good glycaemic control and compliance with

screening and treatment. Vascular disease and renal failure are major causes of increased

morbidity and mortality.

1 Diabetes control and complications trial (DCCT) showed that strict glycaemic control in type 1 diabetes

mellitus # the risk of development and progression of diabetic microvascular complications

0 تعليق

PH.Jafar Jassim 8/07/2020 01:15:00 ص

تابع القراءه