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DMD3 > Surgery for Dentists > Flashcards

Surgery for Dentists Flashcards

1
Q

What are the causes of surgical disorders?

A

Congenital

Or

Acquired:
• Trauma ( mechanical, thermal, chemical, electrical, ionising radiation)
• Inflammation
• Infection
• Neoplasia
• Vascular
• Degenerative
• Metabolic disorders
• Endocrine disorders
• Other abnormalities of tissue growth
• Iatrogenic
• Drugs, toxins, diet, exercise, environment
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2
Q

What kind of congenital defects that require surgery are most common?

A

Cleft lip and palate are among the most common of all birth defects. Others are very rare.

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3
Q

How do congenital defects affect the face/head and what is required as a result?

A

Mostly affect how a person’s face or head looks. These
conditions may also affect other parts of the body.

Treatment depends on the type of problem

Reconstructive surgery may help the person’s
appearance

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4
Q

How common is cleft lip? How common is cleft palate?

A

Cleft lip occurs 1 in 750 live births, cleft palate 1 in every
2000

Half the cleft lip also have a cleft palate

10% patients with cleft have other malformation

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5
Q

What kinds of trauma can result from chemical injuries?

A

Sodium hypochlorite solution commonly used in root canal
treatments (Strongly alkaline with pH 11 to 13)

Complications of accidental spillage are damage to clothing,
damage to eye, damage to skin and damage to oral mucosa

Complications from hypochlorite extrusion into peri-radicular soft tissue include chemical burns and tissue necrosis and
neurological complications like anaesthesia or paraesthesia

Using sodium hypochlorite for root canal irrigation without adequate isolation of the tooth can lead to leakage of the solution into the oral cavity and ingestion or inhalation by the patient, resulting in throat irritation and in severe cases, upper airway compromise

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6
Q

What causes inflammation?

A

Often stems from infection

Can result from physical irritation (noxious chemicals for example)

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7
Q

What causes inflammation of salivary glands?

A

Calculus

Viruses

Bacterial infection

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8
Q

How can infection spread?

A

Bacterial diffuse through the dentinal tubules toward the
pulp and evoke inflammatory changes resulting in pulpitis
and pulp necrosis

Bacteria from the pulp spreads into periapical tissues and soft tissues and bones of the face and neck

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9
Q

What is the metabolic response to injury?

A

Often occurs in 2 phases:

Catabolic phase: High metabolic rate, breakdown of proteins/fats, negative nitrogen balance and weight loss.

Anabolic phase: Protein and fat stores are restored and weight gain (positive nitrogen balance)

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10
Q

What kinds of conditions can diabetes have on the mouth?

A

Periodontal disease

Candidosis

Dry mouth and increased caries

Glossitis

Burning mouth syndrome

Orofacial dysaesthesia

Poor healing

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11
Q

What factors mediate the metabolic response to injury?

A

Acute inflammatory response

Endothelium and blood vessels

Neuroendocrine response

Bacterial infection

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12
Q

What happens during the acute inflammatory response?

A

Injury -> activation of macrophages -> Cytokine release -> Neutrophils + macrophages recruited to site to clear dead tissue and bacteria -> Cytokines in circulation initiate systemic features (IL-1 fever, and acute phase protein IL-6) -> Other pro-inflammatory cytokines released and anti-inflammatory cytokines are also released

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13
Q

What does clinical condition of someone with acute inflammation depend on?

A

Clinical condition of patient depends on extent to which inflammation remains localized and the balance between pro and anti-inflammatory processes

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14
Q

What are the pro inflammatory cytokines released durign the acute inflammatory response?

A

Prostaglandins, kinins, complement, proteases, and free radicals

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15
Q

What anti-inflammatory cytokines are released during the acute inflammatory response?

A

Antioxidants, protease inhibitors, and IL-10

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16
Q

What happens to the endothelium and blood vessels?

A

Expression of adhesion molecules upon endothelium leads to leukocyte adhesion

Release of kinins, prostaglandins and nitric oxide leads to vasodilation and increased local blood flow.

Increased capillary permeability leads to delivery of inflammatory cells, oxygen and nutrient substrates which are important for healing.

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17
Q

What causes adhesion and coagulation during inflammation?

A

Oedema is caused from colloid particles (albumin) leaking into the injured tissues

Coagulation and platelet activation is promoted by exposure of tissue factor.

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18
Q

How does sympathetic activation occur during the acute inflammatory response?

A

Tissue injury and inflammation leads to impulses in afferent pain fibres that reach the thalamus and mediate
metabolic response

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19
Q

What happens when the sympathetic nervous system is activated during the acute inflammatory response?

A

Activation of sympathetic nervous system leads to release of noradrenaline from sympathetic nerve fibre endings and adrenaline from adrenal medulla.

This results in tachycardia, increased cardiac output, and carbohydrate, fat and protein metabolism

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20
Q

What is the neuroendocrine response to acute inflammation?

A

Changes in the circulating

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21
Q

What are the consequences of metabolic response to injury?

A

Hypovolaemia

Increased energy metabolism and substrate cycling

Catabolism and starvation

Changes in red blood cell synthesis and coagulation

Anabolism

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22
Q

What causes hypovolaemia following the acute inflammatory response?

A

Loss of blood, fluid or water.

Sequestration of protein-rich fluid into interstitial space caused by the increased vascular permeability.

Decreased circulating volume will reduce oxygen and nutrient delivery and increased healing and recovery time.

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23
Q

What are the neuroendocrine responses to hypovolaemia?

A

Release of ADG and aldosterone = oliguria + sodium and water retention.

Reduced cardiac preload = Lower cardiac output + decreased blood flow to tissues and organs this results in activation of Sympathetic NS = increased cardiac output, peripheral vasoconstriction and rise in BP.

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24
Q

What happens to BMR following surgery?

A

The overall energy expenditure rises by 50% due to increased generation of heat, fever, and BMR.

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25
Q

How is catabolism different to starvation?

A

Catabolism is a breakdown of complex substances to glucose, amino acids, and fatty acids mediated by increase in catecholamines, cytokines, and hormones.

Total energy expenditure is increased in proportion to injury severity.

Starvation occurs when intake is less than the metabolic demand. Can be acute or chronic.

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26
Q

What patient factors are associated with the magnitude of metabolic response to injury?

A

Genetic predisposition

Coexisting disease

Drugs

Nutritional status

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27
Q

What trauma factors are associated with magnitude of metabolic response to injury?

A

Severity

Nature

Ischaemia-reperfusion

Temperature

Infection

Anaesthetic technique

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28
Q

What changes are seen in red blood cell synthesis and coagulation following surgery?

A

Anaemia is common after major surgery or trauma

Following tissue injury the blood is hypercoagulable and increased risk of thromboembolism

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29
Q

What happens during the anabolism stage following surgery?

A

Regaining of weight

Restoring skeletal muscle mass

Replenishing fat stores

30
Q

Which hormones are released during the anabolism stage following surgery?

A

Insulin

Growth Hormone

Insulin like growth factors

Androgens

31
Q

What is shock?

A

Imbalance between oxygen demands and delivery

32
Q

What does shock do to the body?

A

Results in cell dysfunction and cell death leading to multiple organ failure and death.

33
Q

What are the types of shock?

A

Hypovolemic shock

Septic shock

Cardiogenic shock

Anaphylactic shock

Neurogenic shock

34
Q

How is shock corrected and what happens if this isn’t done?

A

Increased sympathetic activity

Maintain adequate perfusion and oxygen delivery to vital organs

Compensatory mechanisms have limits

Uncorrected shock leads to under-perfusion of organs

Shock leads to up-regulation of pro-inflammatory cytokines, systemic inflammatory response syndrome (SIRS), organ dysfunction and multiple organ failure.

35
Q

What type of shock is most common?

A

Hypovolaemic shock

36
Q

What are the classifications of haemorrhagic shock?

A

Class 1 (<15%) represents a compensated state

Class 2 (15 - 30%)

Class 3 (30 - 40%)

Class 4 (>40%) this is life threatening

37
Q

What are the signs of hypovolaemic shock?

A

Increased pulse rate

Dropping blood pressure

Increased respiratory rate

Reduced urine output

Increased confusion and lethargy

38
Q

How is hypovolaemic shock treated?

A

Arrest of haemorrhage and rapid fluid resuscitation to restore circulating volume

39
Q

What is the sequence of steps from hypovolaemia to death?

A

Hypovolaemia -> Decreased venous return -> Decreased preload -> Decreased CO -> hypotension -> Perfusion failure and tissue hypoxia -> Organ dysfunction -> Multi organ failure

40
Q

What causes septic shock?

A

Sepsis from localized infection with gram +ve and -ve bacteria. Most common sites are lungs, abdomen, urinary tract and skin.

Infection triggers a cytokine-mediated pro-inflammatory response that results in peripheral vasodilation, redistribution of blood flow, endothelial cell activation, increased vascular permiability, and formation of microthrombi within microcirculation.

41
Q

How is septic shock managed?

A

Identification and treatment of underlying infection (antibiotics)

Optimize tissue oxygen delivery (preserve tissue perfusion)

Each hour delay in treatment of sepsis is associated with 8% increase in risk of mortality.

42
Q

What is cardiogenic shock?

A

Heart is unable to maintain cardiac output sufficient to meet metabolic requirements

Caused by myocardial infarction, arrhythmias, valve dysfunction, cardiac tamponade, massive pulmonary embolus, tension pneumothorax

43
Q

How is cardiogenic shock treated?

A

Reverse the cause.

Manage CO (preload, myocardial contractility, HR and afterload)

Careful balance of vasodilator, inotrope and vasoconstriction

Some definitive treatment such as percutaneous coronary intervention, coronary bypass grafting or mitral valve repair.

44
Q

What causes anaphylactic shock?

A

Severe systemic hypersensivity.

Anaphylactic shock results from vasodilation, intravascular volume redistribution, capillary leak and reduction in cardiac output

45
Q

What causes neurogenic shock?

A

Loss of sympathetic tone to vascular smooth muscle injury to spinal cord.

Results in profound vasodilation, fall in systemic vascular resistance and hypotension

46
Q

How is fluid normally distributed in the body?

A

60% of total body weight:

40% is intracellular fluid
20% is extracellular fluid

Fluid crosses compartment to compartment due to hydrostatic and osmotic pressure.

ICF has low Na+ and high K+

ECF has high Na+ and low K+

47
Q

How are fluids managed for surgery?

A

Filling intravascular compartment rapidly is done via using plasma substitute or blood. (fluids with high colloid osmotic potential remain in intravascular space)

A crystalloid solution will distribute over the entire extravascular compartment which is 4x as large as the intravascular compartment.

5% dextrose will redistribute across both intracellular and extracellular space

48
Q

How is fluid typically lost?

A

4 routes:

Kidney (aldosterone + ADH)

GI tract (300ml lost in faeces)

Skin

Resp tract

Skin + respiratory tract together are responsible for 700ml/day

49
Q

What effect does surgery have on electrolytes and fluids?

A

Stress response to surgery is release of ADH and catecholamines and activation of renin-angiotensin system, resulting in oliguria and water retention.

Potassium released by damaged tissues. If renal perfusion is poor and urine output poor, potassium is not excreted and accumulates. Resultant hyperkalaemia causes arrhythmias.

50
Q

How are patients fluid levels made normal following surgery?

A

Majority of patients require fluid replacement for brief period postoperatively until normal diet is resumed.

In severely ill patients and those with impaired GI function, long term nutritional support is necessary.

51
Q

What kind of nutritional support should be given to patients postoperatively?

A

25 - 30 Kcal/Kg/day. The amount of protein depends on patient’s weight, body composition, clinical status, mobility, and dietary intake.

Monitor patients to detect any deficiencies and assess adequacy of energy and protein provision.

52
Q

Why is nutritional support necessary postoperatively?

A

Protein and energy loss leads to slow recovery, poor wound healing and increased infections.

53
Q

How should nutritional support be provided to patients?

A

Nutrients given via GI tract or intravenously. GI tract more ideal.

Enteral feed is safer, cheaper, and maintains gut function (potential immunological and metabolic benefits)

54
Q

What factors are important in the development of infection?

A

Host defence system: Physical barriers, antagonism by commensals, antibacterial substances, immune state, acquired immunity, innate immunity.

Bacterial factors: Virulence, inoculum, growth rate

Insults: Foreign body, necrosis, ischaemia, haematoma

55
Q

How can infection be prevented?

A

Aseptic technique (hand washing, surgical scrub, skin preparation of patient, sterile field, safe operating practices)

Hand decontamination

Personal protective equipment (PPE) (Cap, face mask, eye protection, sterile gown + gloves)

Skin preparation (antiseptics on surgical site prior to incision reducing resident organisms and risks of wound infection)

Surgical instruments (Washer + autoclav)

56
Q

How are prophylactic antibiotics to be given?

A

Aims to prevent infection by achieving high concentrations of it in the blood during surgery.

Must cover likely pathogens. (consider AB resistance)

Single dose of antibiotics usually should be enough for prophylaxis.

57
Q

Should antibiotic prophylaxis be used in dental surgery?

A

Not necessary in immunocompetent patients.

In maxillofacial surgery consider as well as immunocompromised patients.

In patients with high risk of endocarditis required for extraction, perio surgery, replanting avulsed teeth, and other surgery)

58
Q

What are the principles of antibiotic use?

A

MINDME

Microbiology guides therapy

Indications should be evidence based

Narrowest spectrum required

Dosage appropriate to site and type of infection

Minimise duration and therapy

Ensure monotherapy in most situations

59
Q

What cardiac conditions are high risk for endocarditis?

A

Prosthetic cardiac valve or prosthetic material used for valve repair

Previous infective endocarditis

Congenital heart disease (only if it involves unrepaired cyanotic defects or completely repaired defects with prosthetic material/device in initial 6 months)

Cardiac transplantation with development of valvulopathy

Rheumatic heart disease in indigenous Australians

60
Q

How is AB prophylaxis administered?

A

Amoxycillin 2g orally, 1 hour before procedure.

Clindamycin 600mg orally, 1 hour before procedure

61
Q

What investigations can be done to see tumours?

A

CT

MRI

PET-CT

US of cervical lymph nodes

Full blood count

Tumour markers

62
Q

What factors does prognosis of a tumour depend on?

A

Extent of spread

Microscopic appearance

Anatomical situation

General condition of patient

63
Q

What kind of surgery is done often to remove tumours?

A

Wide local resection

Neck dissections

64
Q

What palliative treatment is provided for cancer?

A

Surgery

Radiotherapy

Hormone therapy

Chemotherapy

Analgesics and anti-emetics

Nerve blocks

65
Q

What post operative care should be given to patients following tumour removal surgery?

A

Clinical assessment and monitoring - assess patient’s
colour, pulse, blood pressure, respiratory rate, oxygen saturation, level of consciousness

Respiratory management – maintenance of airway and
adequate ventilation

Cardiovascular management monitor for blood loss

Fluid, electrolyte and renal management

Control of sepsis

Nutrition

66
Q

What are the complications of anaesthesia and surgery?

A

Nausea + vomiting

Resp. complications

Pulmonary collapse and infection. Resp. failure. Acute Respiratory Distress Syndrome

67
Q

What are the complications of anaesthesia and surgery?

A

Risks of anaesthesia and surgery increased in patients
suffering from cardiovascular disease:

  • Myocardial ischaemia/infarction
  • Cardiac failure
  • Arrhythmias
  • Postoperative shock

Cerebral complications –
Cerebrovascular accidents
(precipitated by sudden hypotension during or after surgery in elderly hypertensive patients with severe atherosclerosis):
- Delirium (usually in the elderly on background of
atrophy, precipitated by sedative or hypnotic drugs)
Treatable causes e.g. hypoxia, sepsis, metabolic disturbances)

Patients with pre-existing renal disease: Risk of hypoperfusion leading to renal failure. Hypoxia aggravates this as well as sepsis and nephrotoxic drugs. Mortality in pts with post op renal failure is 50%.

DVT (increases with age, obesity, prolonged operations, pelvic and hip surgery, malignant disease)

Wound infection

Wound dehiscence (Poor technique, local tissue necrosis due to infection, obesity, smoking, renal failure)

68
Q

How can DVT be prevented?

A

Graded compression support stockings, mechanical compression of calf muscles during surgery

69
Q

How can PE from DVT be treated?

A

Immediate CPR, heparinization and urgent CT pulmonary angiopathy.

Fibrinolytic agents IV if at least 6 days post surgery.

Open pulmonary embolectomy under cardiopulmonary bypass.

Warfarin for 6 months

IVC filter if further PE despite anticoagulation or cannot be anticoagulated.

70
Q

What are the signs and symptoms of wound infection?

A

Malaise

Anorexia

Pain

Discomfort

Local erythema

Tenderness

Swelling

Cellulitis

Wound discharge

Abscess formation

71
Q

What should be used to treat infection as a complication of surgery?

A

Antibiotics if evidence of associated cellulitis or septicaemia

DMD3 (53 decks)

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