Management of medically

compromised patients. 1

Dr. Alaa S. Taha

MSc. OMFS.
Learning objectives
Understand the concept of compromised patients.
Understand the aspects of managing patients with
diabetes mellitus.
Terminologies
Medically Compromised Patient.
Physically Compromised Patient.
Emergency (intervention within 1 hr).
Urgency (intervention within 24 h).
Scheduled procedure.
Elective procedure.
Diabetes Mellitus.
DM
Ebers Papyrus, 3000 and 1500 BC.
Definition
Its a metabolic disorder characterized by a sustained
high blood glucose level resulting from an absolute or
a relative lack of insulin, and / or diminished
effectiveness of circulating insulin (insulin
resistance).
Pathophysiology
All ingested carbohydrate are digested into glucose.
Glucose homeostasis depends mainly on the
pancreatic hormones;
Insulin:
from beta-cells of the islets of Langerhans.
Glucagon:
from the alpha-cells in the islets.
Amylin:
from beta-cells of the islets.
Insulin
Enhances peripheral glucose uptake.
Inhibits breakdown of liver glycogen.
Enhances storage of glucose as glycogen.
Increases protein synthesis.
Increases triglyceride storage.
Glucagon
Stimulates the liver to convert glycogen into glucose,
thus raising glucose levels.
Have the opposite effect to insulin.
Amyline
Modulates gastric emptying and satiety and decreases
the postprandial rise in glucagon.
Several other hormones that can influence glucose
include catecholamines (adrenaline and
noradrenaline), corticosteroids, thyroid hormone,
growth hormone, estrogen and progesteron.
Pathophysiology cont.
In diabetes, with insulin lacking or its action blocked,
glucose cannot enter cells and, without energy,
weakness results (lethergy). Glucose also then
accumulates in the blood (hyperglycemia) and spills
over into the urine (glucosuria), taking with it
osmotically a large amount of water (polyuria), This
leads to dehydration and thus thirst and the need to
drink excessively (polydipsia).
As glucose is then no longer a viable energy source,
fat and protein stores are metabolized with weight
loss, peripheral muscle wasting and in type 1
diabetes the production of ketone bodies (eg:
acetone).
In severe cases, ketone bodies may be detected on the
breath, and accumulate in the blood (ketonaemia) as
well as be excreted in the urine (ketonuria). The
resultant metabolic ketoacidosis leads to a
compensatory increase in respiratory rate
(hyperventilation) and a secondary respiratory
alkalosis.
Chronic hyperglycemia causes microvascular
complications and atherosclerosis, leading to:
Hypoglycemia / hyperglycemia.
Hyper Osmolar Non Ketotic coma.
Diabetic keto acidosis (DKA).
Neuropathy (pripheral / autonomic).
Retinopathy.
Nephropathy (Renal failure).
Peripheral arterial angiopathy.
Cardiovascular diseases.
Cerebrovascular diseases.
Classification
Type I diabetes.
Type II diabetes.
Gestational diabetes.
Secondary diabetes.
Type 1 diabetes
insulin-dependent (IDDM) or
juvenile-onset diabetes
most commonly diagnosed at about 12 years of age
and commonly presents before the third decade.
Characterized by antibodies directed against insulin
and the pancreatic islets of Langerhans.
Latent auto immune diabetes in adults (LADA) is
essentially a slow presentation of type 1 diabetes, which is
seen in slimmer patients who progress quickly to insulin
requirement.
Anti-GAD (glutamic acid decarboxylase) antibodies may
be helpful in the diagnosis.
Symptoms usually develop over a short period.
Diabetic ketoacidosis coma is a significant risk.
Insulin is required daily for life, and diet must be
controlled.
Hypoglycemia is also a risk.
Type 2 diabetes
non-insulin-dependent
(NIDDM) or maturity-onset
diabetes
most commonly diagnosed above the age of 40.
Patients are typically overweight.
Patients are insulin resistant and have diminished
beta-cell function.
Maturity-onset diabetes of the young (MODY) is
caused by autosomal dominant mutations and so there
is vertical transmission of diabetes within families.
The phenotype varies from mild glucose intolerance
to insulin-requiring diabetes, typically diagnosed
before the age of 25 years.
Symptoms usually develop gradually.
Most patients with type 2 diabetes can be managed on
diet and oral hypoglycemic drugs. However many will
eventually need insulin, but are often resistant.
About 80% of people with type 2 diabetes have the
metabolic syndrome that includes obesity, elevated
blood pressure and high levels of blood lipids.
Gestational diabetes
Its basically an insulin resistance state that appears
usually in the second or third trimester of pregnancy.
Estrogen typically increases cells’ response to insulin,
and progesterone makes them more resistant.
Most common in people of African heritage or with a
family history of diabetes.
Carries an increased risk of type 2 diabetes later.
Secondary
• usually secondary to:
Steroids.
Thiazide Diuretics.
Drugs for HIV.
Pancreatectomy.
Acute pancreatitis and Chronic Pancreatitis.
Hemochromatosis.
Cystic Fibrosis.
Cushing's Disease.
Acromegaly.
Signs and Symptoms
Lethargy / tiredness.
Polyuria.
Thirst / Polydypsia.
Weight loss.
Recurrent skin, oral and genital infections
Confusion/ aggression/ behavioral changes/
Irritability.
Abdominal pain/ nausea and vomiting.
Ketoacidosis.
Visual deterioration.
Paraesthesia (hands and feet).
Renal failure.
Coma.
Oral Manifestations
Severe periodontitis.
oral candidosis.
Mucormycosis in the paranasal sinuses and nose.
Severe dentoalveolar abscesses with fascial space
involvement.
Circumoral paraesthesia (important sign of
impending hypoglycaemia).
Cranial nerve deficits (occasionally).
Sialosis (occasionally).
Temporary lingual and labial paraesthesia may follow
the removal of mandibular third molar teeth.
Burning mouth sensation in the absence of physical
changes.
Dry mouth.
The ‘Grinspan syndrome’ (diabetes, lichen planus and
hypertension). coincidental?!!!
Lab. Investigations
Test Confirmed Excluded
diabetic diabetic

Fasting plasma glucose > 7.0 mmol/L < 6 mmol/L

(after a person has fasted (126 md/dl)
for 8 h)

Random blood glucose ≥ 11.1 < 8 mmol/L

(taken any time of day) mmol/L (200
mg/dl)
Test Confirmed Excluded
diabetic diabetic

oral glucose tolerance test > 11.1 < 11.1

Plasma (glucose taken 2 h mmol/L mmol/L
after a person has consumed a
drink containing 75 g of
glucose in) (OGTT)

Hb
A1CC
Diagnosis
Blood glucose levels - venous samples:
1 sample is diagnostic if symptomatic.
2 samples if a symptomatic.
Screening at Risk People
• Whom to screen:
BMI>30.
Age >50.
Family history.
GDM.
•How to screen:
Urinalysis.
FBG.
Random blood glucose.
OGTT.
Hb A1C.
Medical management
Diet and Exercise.
Oral hypoglycaemic therapy:
eg; Biguanides (Metformin)
Sulphonylureas (glibenclamide)
Insulin Therapy:
eg; Long acting Insulin.
Short acting Insulin.
Mixed Insulins.
Others:
eg; Anti hypertensive.
Aspirin.
Statins.
Dental management <5mmol/l,
Pre operative assessment. 180mg/dl
Time and setting of Surgery.
Diet.
Blood Glucose Level at the Time of Surgery
Pre / post operative antibiotics.
Management of dental and fascial infections.
Administration of Local Anesthetics.
Administration of Conscious sedation with
benzodiazepines.
Administration of Other Drugs (acetaminophen,
salicylates, anxiolytics, doxycycline, tetracyclines
and ciprofloxacin).

Aspirin ABs enhance

agonize insulin effect
antidiabetics
Autonomic neuropathy in diabetes can cause
orthostatic hypotension; therefore the supine patient
should be slowly raised upright in the dental chair.
Wound care.
Dental Office Supplies
Diabetics controlled by insulin
The desired whole blood glucose level is 3–5
mmol/L. For major surgery,
The effects of stress and trauma may raise insulin
requirements and precipitate ketosis.
Preoperatively the patient should be put on soluble
insulin and stabilized.
At 8.00–9.00 am blood should be taken for glucose
estimation and an intravenous infusion set up giving
glucose 10 g, soluble insulin 2 units and potassium 2
mmol/h (GIK infusion), until normal oral feeding is
resumed – at which time the patient can be returned to
the pre-operative insulin regimen.
Blood glucose should be monitored at 2–4-hour
intervals until the patient is feeding normally.
The patient is put on an insulin sliding scale from the
morning of the day of operation until the normal
feeding regimen is possible.
Autonomic neuropathy can lead to postural
hypotension and impaired ability to respond to
hypoglycemia, and carries a risk of cardiorespiratory
arrest under GA.
Diabetics controlled by diet only
Dental treatment can be carried out without special
precautions apart from monitoring the blood glucose
before the operation, on recovery, and at 2-hours
intervals.
Poorly controlled diabetics with raised fasting
glucose levels, should be referred for improved
control of their blood glucose before elective surgery
is performed. If emergency surgery is needed, then
prophylactic antibiotics are recommended .
Diabetics controlled by diet and oral
hypoglycemic
Well controlled patients can safely have short simple
procedures carried out under GA in hospital without
insulin, but the blood glucose should be monitored 2-
hourly.
If diabetic control is poor, if the patient is on large
doses of drugs or if more major surgery is planned, a
suggested regimen is as follows:
Pre-operative assessment and stabilization.
Metformin must be stopped at least 2 days
preoperatively because of the risk of lactic acidosis if
contrast media are being used.
At 8.00–9.00 am on the day of operation, blood is
taken for glucose estimation and an intravenous
infusion line is put up.
 Infusion of 10% glucose (500 ml) containing 10
mmol potassium chloride and insulin 5 units (if the
blood glucose is < 6 mmol/L) or insulin 10 units (if
the blood glucose is > 6 mmol/L) is continued at 100
ml/h until normal food can be taken orally.
The blood glucose is monitored regularly.
The infusion is stopped when patient resume oral
feeding and the oral hypoglycemics are restarted.
Hypoglycaemia < 2.5mmol/l
55 mg/100 ml
• Causes:
Too much insulin.
Food omission.
Sulphonylureas.
Renal impairment.
Signs and symptoms:
Hunger.
Distress / anxiety.
Fatigue.
Sweating.
Vertigo.
Trembling.
 Pallor.
Headache/ mental confusion.
Paresthesia.
Diplopia and blurred or decreased vision.
Convulsions.
loss of consciousness, coma, and death.
Management:
If the patient is conscious give glucose
solution or gel immediately by mouth or 10 g sugar.
If the patient is comatose give 10–20 ml of 20-
50% sterile dextrose intravenously or if a vein cannot
readily be found, glucagon 1 mg intramuscularly.
On arousal, the patient should also be given
glucose orally usually in the form of longer-acting
carbohydrate (e.g. bread, biscuits).
Hyperglycemia
Diabetic hyperglycemia develops slowly, observed
more rarely, and is less dangerous than hypoglycemia.
It is characterized by weakness, headache, nausea,
vomiting, diarrhea, hyperventilation, ketonuria,
acetone breath, xerostomia, dehydration, dyspnea,
hypotension, tachycardia and, finally, lethargy
resulting in a coma.
Caused by too little insulin, infection, or myocardial
infarct.
Management
Hyper osmolar non ketotic coma
Seen in type II diabetics.
Patient is usually unwell for days
There is no acidosis or ketones but a very high blood
glucose level.
Carries a high risk of clotting. Management:
Fluids, Insulin,
Potassium,
Heparin
Diabetic Keto Acidosis
• Causes:
Infection
Omits insulin
Dehydration
• Signs and symptoms:
Management:
Keton bodies. Fluids, Insulin,
Hyperventilation. Potassium,
Hypotension. Antibiotics.
Tachycardia.
Coma.
Suggested readings:
Medical problems in dentistry, skully.
Oral surgery, Fragisco.
Any questions?!!