PSORIASIS
The familiar pink or red lesions with a scaling surface and well defined edge are easily recognized. These changes can be related to the histological appearance:
1. The increased thickness of the epidermis, presence of nuclei above the basal layer, and thick keratin are related to increased epidermal turnover.
2. Because the epidermis is dividing it does not differentiate adequately into normal keratin scales. These are readily removed to reveal the tortuous blood vessels beneath – clinically, “Auspitz sign”. The psoriatic plaque can be likened to a brick wall badly built by a workman in too much of a hurry – it may be high but it is easily knocked down.
3. The polymorphs that migrate into the epidermis from sterile pustules in pustular psoriasis. These are most commonly seen on the palms and soles.
4. The dilated blood vessels can be a main feature, giving the clinical picture of intense erythem.
The equivalent changes in the nail cause thickening and “pits” 0.5 – 1.0 mm in diameter on the upper nail plate that then fall out. Onycholysis, in which the nail plate is raised up, also occurs in psoriasis.
While still considering the individual lesion remember the following points.
The size or the lesion varies from a few millimeters to very extensive plaques.
Scaling may predominate, giving a thick plaue, which is sometimes hence the name “rupioid.” Scratching the surface produces a waxy appearance – the “tache de bougie” (literally “a line of candle wax”).
Erythema may be conspicuous, especially in lesions on the trunk and flexures.
Pustules are rare on the trunk and limbs, but deep seated pustules on the palms and soles are fairly common.
Psoriasis usually occur in early adult life, but the onset can be at any time from infancy to old age, when the appearance is often atypical. The following factors in the history may help in making a diagnosis:
· There may be a family history – if one parent has psoriasis 16% of the children will have it, if both parents the figure is 50%.
· The onset can occur after any type of stress, including infection, trauma, or childbirth.
· The lesions may first appear at sites of minor trauma – Köebner’s and toes or phenomenon
· The lesions usually clear on exposure to the sun
· Typically, psoriasis does not itch
· There may be associated arthropathy – affecting either the fingers and toes or a single large joint.
Clinical Presentation
Patients usually present with plaques and sometimes annular lesions on the elbows, Köbner’s phenomenon with lesions developing in areas of skin trauma such as scars or minor scratches. Normal everyday trauma such as handling heavy machinery may produce hyperkeratotic lesions on the palms. In the scalp there is scaling, sometimes producing very thick accretions. Erythema often extends beyond the hair margin. The nails show “pits” and also thickening with separation of the nail from the nail bed (oncholysis).
Guttate psoriasis – from the Latin gutta, a drop – consists of widespread small pink macules that look like drops of paint. It usually occurs in adolescents and often follows an acute ß haemolytic streptococcal infection. There may be much distress to both parent and child when a previously healthy adolescent erupts in apparent leprous spots.
Pustular lesions occur as chronic deep seated lesions on the palms and soles with surrounding Erythema which develop a brown colour and scaling. In clinics north of the border these pustules make the patient ask whether the condition is “smitten’ – that is, infectious. It is important always to explain that it is not.
Flexural psoriasis produces well defined erythematous areas in the axillae and groins and beneath the breasts. Scaling is minimal or absent.
Napkin psoriasis in children may present with typical psoriatic lesions or a more diffuse erythematous eruption with exudative rather than scaling lesions.
Generalised pustular psoriasis is uncommon. Superficial pustules develop in an area of intense erythema
Erythrodermic psoriasis is a serious, even life threatening, condition with erythema affecting nearly the whole of the skin. Diagnosis may not be easy as the characteristic scaling of psoriasis is absent, although this usually precedes the erythroderma. Less commonly the erythema develops suddenly without the erythema develops suddently without preceding lesions. There is a considerable increase in cutaneous blood flow, heat loss, metabolism, and water loss.
It is important to distinguish between the stable, chronic, plaque type of psoriasis, which is unlikely to develop exacerbations and responds to tar, dithranol, and ultraviolet treatment, and the more acute erythematous type, which is unstable and likely to spread rapidly, particularly when irritated by tar, dithranol, or ultraviolet light.
Patients with seronegative arthropathy of the non-rheumatoid type show double the normal (2%) incidence of psoriasis. Psoriatic arthropathy commonly affects the distal interphalangeal joints, sparing the metacarpophalangeal joints, and is usually asymmetrical. Rheumatoid nodules are absent. The sex ratio is equal but a few patients develop a “rheumatoid like” arthropathy, which is more common in women than in men. There is a third rare group who suffer bones.
Other members of the families of those with psoriatic arthropathy are affected in 40% of cases. There may be severe pustular psoriasis of the fingers and toes associated with arthropathy. One patient was so severely affected that she was immobilized until her condition cleared on treatment with methotrexate.
The cause is unknown but there is an inherited predisposition. Local trauma, acute illness, and stress may be factors in causing the appearance of clinical lesions. ß haemolytic streptococcal throat infection is a common precipitating factor in guttate psoriasis. Antimalarial drugs, lithium, and ß blockers can make psoriasis worse. There is evidence that psoriasis occurs more radily and is more intractable in patients with a high intake of alcohol. Smoking is associated with palmo-plantar pustulosis.
There is evidence that both hormonal and immunological mechanisms are involved at a cellular level. The raised concentrations of metabolites of arachodonic acid in the affected skin of people with psoriasis are related to the clinical changes. Prostaglandins cause erythema, while leukotrienes (LTB4 and 12 HETE) cause neutrophils to accumulate. The common precursor of these factors is phospholipase A2, which is influenced by calmodulin, a cellular receptor protein for calcium. Both phospholipase A2 and calmodulin concentrations are raised in psoriatic lesions.
T helper lymphocytes have been found in the dermis as well as antibodies to the basal cell nuclei of psoriatic skin. There are also dermal factors that contribute to the development of psoriatic lesions. The detailed treatment of psoriasis is covered in the next lesions. The only point to be made here is the importance of encouraging a positive attitude with expectation of improvement but not a permanent cure, since psoriasis can recur at any time. Some patients are minor lesions are a catastrophe.
Abnormalities found in psoriatic skin with possible explanations
Abnormalities
Comment
Accelerated transit time of keratinocytes through the epidermis
The most consistent observation in psoriatic skin.
Increased mitotic activity
Increased rate of DNA synthesis
Not only the basal layer keratinocytes, but also cells two or three layer above
Increased levels of phospholipase A2 activity
Availability of fee arachidonic acid High levels LTB4 may explain pustules in psoriatic lesions
Elevated levels of polyamine synthesis
May well be secondary to rapid cell proliferation
Increased levels of plasminogen activator
May explain Koebner phenomenon
Presence of keratins 6 and 16 in epidermis
Probably secondary to accelerated transit time.
Increased cGMP levels leading to high ration Cgmp/Camp
High levels of calcium binding protein calmodulin
Both cyclosporine and dithranol are calmodulin antagonists
Sunday, October 28, 2007
Skin Lesions by Dr. Azar Rsheed
SKIN LESIONS
(A) ANATOMY OF SKIN
SKIN: The largest organ in the body (16% of total body weight).
Composed of (i) Stratified cellular epidermis.
(ii) Underlying dermis of connective tissue resting on adipose hypodermis.
Epidermis: Approximately 0.2 mm thick. Five layers from within outwards.
(i) Stratum germinativum – (basal cell layer) – single layer of tall columnar, basophilic cells with large nuclei.
Scattered in between are dendritic cells (melanocytes) producing melanin.
(ii) Stratum Malpighii – (prickle cell layer or acanthotic layer) – Several cells deep. Polygonal, squamous cells sticking to each other by means of intercellular bridges called prickles (acanthus).
(iii) Stratum granulosm – rreansversely-lying cells containing keratophalin granules.
(iv) Stratum lucidum – clear zone found in palms and soles only.
(v) Stratum corneum (Horny layer)- several rows of anucleate, cornfiied cells. Average time taken by a cell from stratum germinativum to its loss from stratum corneum is 28 days.
Thickest on palms and soles and thinnest on eyelids. Acts as barrier to absorption
Dermis. Approximately 1.8 thick. Compsed of ground substance largely comprising of mucopolysaccharides. In its are scattered:
1. Cells e.g. fibroblasts (producing fibrinous collagen), mast cells (producing histamine) and histiocytes (reticulo-endothelial cells).
2. Fibres e.g. collagen, reticular and elastic. All from interlacing network giving strength and elasticity to the dermis.
3. Sweat Glands: (i) Eccrine – Found all over the body.
(ii) Apocrine – Found only in axillae, breasts and genital
region. Functional ast puberty.
4. Sebaceous Glands: Holocrine organs producing sebum.
5. Hair follicles with tangentially situated arrector pili muscles.
6. Blood vessels e.g. capillaries, arterioles and venules.
7. Lymphatics.
8. Nerves (i) Motor – Autonomic
(ii) Sensory – Free and encapsulated nerve endings.
SPECIALISED ECTODERMAL STRUCTURES: (Adaptation of horny layer).
1. Hair – Human body contains some five million hair follicles, number reducing with advancing age. Average rate of growth on scalp 3 millimeter per week. Three types:
(i) Lanugo – Downy, soft and unmedllated. Shed in utero.
(ii) Vellus – Fine, soft, unmedullated and unpigmented. Gradualy replaced after puberty by terminal hair.
(iii) Terminal – Longer, coarser, medullated and pigmented. Cycles of hair growth are asynchronous i.e. at a given time some hair are growing while others are resting or falling. One loses 50-100 hair/day normally from scalp. Total hair on scalp number 100,000 on average.
2. Nails: Formed from an invagination of epidermis situated on the dorsum of distal phalanx. Average rate of growth half to one mm/week. The toenails grow slower than finger nails.
(B) FUNCTIONS OF SKIN
1. Protection : Against mechanical, microbial, physical
or chemical injury
2. Water & Electrolyte : Through perspiration
regulation
3. Heat regulation : By means of sweating and variations in caliber of
blood vessels.
4. Perception : Of touch, pain and temperature.
5. Excretion : Of waste products e.g. urea, lactic acid.
6. Manufacture : Of Vitamin D.
7. Aesthetic : Attraction for the opposite sex.
8. Emotional : e.g. flushed in anger, pale in fear.
(C) TYPES OF SKIN LESIONS
(i) Primary – Those arising on normal skin.
(ii) Secondary – Superimposed on an already existing skin lesions.
1. Visible but impalpable alterations:
Macule : (Literally a spot) Change in the colour different from its
surrounding skin e.g. freckle.
Patch : Larger lesion of same sort e.g. melasma.
2. Palpable and usually visible alterations:
Papule : Lesion less than one centimeter in size having length.
Breadth and elevation e.g. lichen planus.
Plaque : Large lesion of same kind e.g. lupus vulgaris.
Nodule : Circumscribed swelling within the substance of the skin e.g. erythema nodosum.
Tumour : Large swelling e.g. squamous cell carcinoma.
Weal : (Derived from wale meaning lash): transient swelling due to oedema of the
dermis e.g. urticaria.
3. Wet or fluid containing lesions:
Vesicle : Fluid containing lesion less than 1 cm in size e.g. pemphigus vulgaris.
Bulla (Blister) : Larger fluid containing lesion e.g. pemphigoid.
Pustule : Pus containing lesion e.g. pustular psoriasis
Weeping : Exudation of fluid from the skin surface consequent upon the loss of superficial
part of the epidermis e.g. eczema.
Crust (Scab) : Produced by exudation of serum, blood or pus which then dries and sticks to the surface e.g. impetigo.
4. Lesions concerning stratum corneum:
Scale : Desquamating horny flake seen in conditions resulting in abnormal keratinisation e.g. psoriasis.
Exfoliation : Universal and continuous shedding of scales e.g. exfoliative dermatitis.
Hyperkeratosis : Hypertrophy of the stratum corneum e.g. chronic eczema.
Ichthyosis : Pattern on the skin surface fancifully resembling fish scales e.g. ichthyosis vulgaris.
5. lesions secondary to skin damage:
Excoriation : Mark, usually linear, produced by scratching e.g. pruritus.
Ulcer : Raw area resulting from loss of skin surface e.g. varicose ulcer.
Erosion : Superficial break in skin involving epidermis only e.g. pemphigus vulgaris
Fissure : Crack in the skin surface when it becomes thickened and inelastic e.g. chronic eczema.
Scare : Fibrous tissue replacement of normal skin often seen as an end result of many skin diseases e.g. burns.
Lichenification: Appearances resulting from thickening of the epidermis characterized by exaggeration of the skin markings and leathery appearance of the skin e.g. lichen simplex.
6. Lesions concerned with blood vessels:
Erythema : Redness due to dialation of blood vessels e.g. rosacea.
Telangiectasis : Pattern produced by permanently dilated blood vessesl e.g. radiodermatitis.
Purpura : Purplish red circumscribed spots due to leakage of blood into dermis e.g. anaphylactoid purpura. (Purpuric lesions do not fade on pressure).
Ecchymosis : Diffuse leakage of blood into dermis on a larger scale than purpura e.g. scurvy.
(Bruising)
Gangrene : Tissue necrosis often as the end result of deprivation of arterial blood e.g. peripheral vascular disease.
7. Special lesions:
Burrow : Seen only in scabies. Greyish, linear, C or S-shaped tunnel, formed by the female sacroptes in the upper epidermis, occurring in characteristics sites.
Comedo (Blackhead): Small black dot plugging the mouth of hair follicle e.g. acne vulgaris.
(D) HISTOPATHOLOGICAL TERMS
(i) EPIDERMAL CHANGES
(1) Hyperkeratosis: Increase in the thickness of stratum corneum.
(2) Parakeratosis: Retension of nuclei in the stratum corneum.
(3) Dyskeratosis: Premature keratinisation of cells.
(4) Granulosis: Increase in the thickness of the granular layer.
(5) Acanthosis: Increase in the thickness of acanthotic layer (Prickle cell layer).
(6) Acantholysis: Loss of intercellular bridges in the prickle cell layer resulting in free floating cells. Characteristically seen in pemphigus vulgaris.
(7) Spongiosis: Intercellular oedema of epidermal cells resulting in a spongy appearance.
(8) Basal Cell: Degenerative process of basal cell layer in which intra and
Liquefaction intercellular vacuolation occurs.
(9) Karyorrhexis: Fragmentation of the nucleus associated with cellular death.
(10) Pyknosis: Shrinking and condensation of the nucleus.
(ii) DERMAL CHANGES
(1) Vascualr : e.g. dilation, necrosis of the vessel wall, oedema.
(2) Cellular
infiltration: e.g. polymorphonuclear, lymphocytic, eosinophilic, histiocytic.
(3) Hypertrophy: e.g. keloid.
(4) Necrobiosis : Loss of nuclei in connective tissue with change in the normal staining
properties.
(5) Granuloma
Formation: Subacute or chronic inflammatory process in which the cellular infiltrate tends to form follicular masses.
(6) Deposits: e.g. fat in xanthomatosis, tattooing pigments.
(7) Tumour
Formation: Benign e.g. fibroma, neuroma, myoma, haemangioma, lymphangioma.
Malignant e.g. squamous cell carcinoma, basal cell carcinoma, melanoma, sarcoma.
(A) ANATOMY OF SKIN
SKIN: The largest organ in the body (16% of total body weight).
Composed of (i) Stratified cellular epidermis.
(ii) Underlying dermis of connective tissue resting on adipose hypodermis.
Epidermis: Approximately 0.2 mm thick. Five layers from within outwards.
(i) Stratum germinativum – (basal cell layer) – single layer of tall columnar, basophilic cells with large nuclei.
Scattered in between are dendritic cells (melanocytes) producing melanin.
(ii) Stratum Malpighii – (prickle cell layer or acanthotic layer) – Several cells deep. Polygonal, squamous cells sticking to each other by means of intercellular bridges called prickles (acanthus).
(iii) Stratum granulosm – rreansversely-lying cells containing keratophalin granules.
(iv) Stratum lucidum – clear zone found in palms and soles only.
(v) Stratum corneum (Horny layer)- several rows of anucleate, cornfiied cells. Average time taken by a cell from stratum germinativum to its loss from stratum corneum is 28 days.
Thickest on palms and soles and thinnest on eyelids. Acts as barrier to absorption
Dermis. Approximately 1.8 thick. Compsed of ground substance largely comprising of mucopolysaccharides. In its are scattered:
1. Cells e.g. fibroblasts (producing fibrinous collagen), mast cells (producing histamine) and histiocytes (reticulo-endothelial cells).
2. Fibres e.g. collagen, reticular and elastic. All from interlacing network giving strength and elasticity to the dermis.
3. Sweat Glands: (i) Eccrine – Found all over the body.
(ii) Apocrine – Found only in axillae, breasts and genital
region. Functional ast puberty.
4. Sebaceous Glands: Holocrine organs producing sebum.
5. Hair follicles with tangentially situated arrector pili muscles.
6. Blood vessels e.g. capillaries, arterioles and venules.
7. Lymphatics.
8. Nerves (i) Motor – Autonomic
(ii) Sensory – Free and encapsulated nerve endings.
SPECIALISED ECTODERMAL STRUCTURES: (Adaptation of horny layer).
1. Hair – Human body contains some five million hair follicles, number reducing with advancing age. Average rate of growth on scalp 3 millimeter per week. Three types:
(i) Lanugo – Downy, soft and unmedllated. Shed in utero.
(ii) Vellus – Fine, soft, unmedullated and unpigmented. Gradualy replaced after puberty by terminal hair.
(iii) Terminal – Longer, coarser, medullated and pigmented. Cycles of hair growth are asynchronous i.e. at a given time some hair are growing while others are resting or falling. One loses 50-100 hair/day normally from scalp. Total hair on scalp number 100,000 on average.
2. Nails: Formed from an invagination of epidermis situated on the dorsum of distal phalanx. Average rate of growth half to one mm/week. The toenails grow slower than finger nails.
(B) FUNCTIONS OF SKIN
1. Protection : Against mechanical, microbial, physical
or chemical injury
2. Water & Electrolyte : Through perspiration
regulation
3. Heat regulation : By means of sweating and variations in caliber of
blood vessels.
4. Perception : Of touch, pain and temperature.
5. Excretion : Of waste products e.g. urea, lactic acid.
6. Manufacture : Of Vitamin D.
7. Aesthetic : Attraction for the opposite sex.
8. Emotional : e.g. flushed in anger, pale in fear.
(C) TYPES OF SKIN LESIONS
(i) Primary – Those arising on normal skin.
(ii) Secondary – Superimposed on an already existing skin lesions.
1. Visible but impalpable alterations:
Macule : (Literally a spot) Change in the colour different from its
surrounding skin e.g. freckle.
Patch : Larger lesion of same sort e.g. melasma.
2. Palpable and usually visible alterations:
Papule : Lesion less than one centimeter in size having length.
Breadth and elevation e.g. lichen planus.
Plaque : Large lesion of same kind e.g. lupus vulgaris.
Nodule : Circumscribed swelling within the substance of the skin e.g. erythema nodosum.
Tumour : Large swelling e.g. squamous cell carcinoma.
Weal : (Derived from wale meaning lash): transient swelling due to oedema of the
dermis e.g. urticaria.
3. Wet or fluid containing lesions:
Vesicle : Fluid containing lesion less than 1 cm in size e.g. pemphigus vulgaris.
Bulla (Blister) : Larger fluid containing lesion e.g. pemphigoid.
Pustule : Pus containing lesion e.g. pustular psoriasis
Weeping : Exudation of fluid from the skin surface consequent upon the loss of superficial
part of the epidermis e.g. eczema.
Crust (Scab) : Produced by exudation of serum, blood or pus which then dries and sticks to the surface e.g. impetigo.
4. Lesions concerning stratum corneum:
Scale : Desquamating horny flake seen in conditions resulting in abnormal keratinisation e.g. psoriasis.
Exfoliation : Universal and continuous shedding of scales e.g. exfoliative dermatitis.
Hyperkeratosis : Hypertrophy of the stratum corneum e.g. chronic eczema.
Ichthyosis : Pattern on the skin surface fancifully resembling fish scales e.g. ichthyosis vulgaris.
5. lesions secondary to skin damage:
Excoriation : Mark, usually linear, produced by scratching e.g. pruritus.
Ulcer : Raw area resulting from loss of skin surface e.g. varicose ulcer.
Erosion : Superficial break in skin involving epidermis only e.g. pemphigus vulgaris
Fissure : Crack in the skin surface when it becomes thickened and inelastic e.g. chronic eczema.
Scare : Fibrous tissue replacement of normal skin often seen as an end result of many skin diseases e.g. burns.
Lichenification: Appearances resulting from thickening of the epidermis characterized by exaggeration of the skin markings and leathery appearance of the skin e.g. lichen simplex.
6. Lesions concerned with blood vessels:
Erythema : Redness due to dialation of blood vessels e.g. rosacea.
Telangiectasis : Pattern produced by permanently dilated blood vessesl e.g. radiodermatitis.
Purpura : Purplish red circumscribed spots due to leakage of blood into dermis e.g. anaphylactoid purpura. (Purpuric lesions do not fade on pressure).
Ecchymosis : Diffuse leakage of blood into dermis on a larger scale than purpura e.g. scurvy.
(Bruising)
Gangrene : Tissue necrosis often as the end result of deprivation of arterial blood e.g. peripheral vascular disease.
7. Special lesions:
Burrow : Seen only in scabies. Greyish, linear, C or S-shaped tunnel, formed by the female sacroptes in the upper epidermis, occurring in characteristics sites.
Comedo (Blackhead): Small black dot plugging the mouth of hair follicle e.g. acne vulgaris.
(D) HISTOPATHOLOGICAL TERMS
(i) EPIDERMAL CHANGES
(1) Hyperkeratosis: Increase in the thickness of stratum corneum.
(2) Parakeratosis: Retension of nuclei in the stratum corneum.
(3) Dyskeratosis: Premature keratinisation of cells.
(4) Granulosis: Increase in the thickness of the granular layer.
(5) Acanthosis: Increase in the thickness of acanthotic layer (Prickle cell layer).
(6) Acantholysis: Loss of intercellular bridges in the prickle cell layer resulting in free floating cells. Characteristically seen in pemphigus vulgaris.
(7) Spongiosis: Intercellular oedema of epidermal cells resulting in a spongy appearance.
(8) Basal Cell: Degenerative process of basal cell layer in which intra and
Liquefaction intercellular vacuolation occurs.
(9) Karyorrhexis: Fragmentation of the nucleus associated with cellular death.
(10) Pyknosis: Shrinking and condensation of the nucleus.
(ii) DERMAL CHANGES
(1) Vascualr : e.g. dilation, necrosis of the vessel wall, oedema.
(2) Cellular
infiltration: e.g. polymorphonuclear, lymphocytic, eosinophilic, histiocytic.
(3) Hypertrophy: e.g. keloid.
(4) Necrobiosis : Loss of nuclei in connective tissue with change in the normal staining
properties.
(5) Granuloma
Formation: Subacute or chronic inflammatory process in which the cellular infiltrate tends to form follicular masses.
(6) Deposits: e.g. fat in xanthomatosis, tattooing pigments.
(7) Tumour
Formation: Benign e.g. fibroma, neuroma, myoma, haemangioma, lymphangioma.
Malignant e.g. squamous cell carcinoma, basal cell carcinoma, melanoma, sarcoma.
Diseases of Pericardium, by Dr. Sultan Mehmood
A 50 YRS OLD MAN PRESENTED WITH ILL HEALTH , ANOREXIA, LOW GRADE FEVER, WT. LOSS, PRECARDIALPAIN AND MILD DYSPNOEA FOR THE LAST 2 MONTHS.HIS PULSE WAS 110 BPM WITH MARKED PULSUS PARADOXUS,JVP 8CM VERTCALLY ABOVE STERNAL ANGLE. HEPATIC ENLARGEMNT 5CM, ASCITES AND PEDAL OEDEMA. HT. SOUNDS WERE FAINTLY AUDIBLE and LUNGS WERE CLEAR.
Q1. WHAT IS THE MOST LIKELY CLINICAL DIAGNOSIS
Q2. WHAT IS THE MOST LIKELY ETILOGICAL
DIAGNOSIS
Q3. WHAT WILL BE THE MOST HELPFUL IMEDIATE
INVESTIGATION
DISEASES OF PERICARDIUM
NORMAL PERICARDIUM
ØLUBRICATES THE SURFACE OF THE HEART
ØPREVENTS SUDDEN DEFORMATION OF THE HEART
ØACTS AS A BARRIER TO THE SPREAD OF INFECTION
ØPREVENTS DISLOCATION OF THE HEART
CLINICAL PRESENTATION OF PERICARDIAL DISEASE
1.ACUTE PERICARDITIS
2. PERICARDIAL EFFUSION
3. CONSTRICTIVE PERICARDITIS
CLASSIFICATION OF PERICARDITIS
•CLINICAL CLASSIFICATION
A. ACUTE PERICARDITIS (< 6 WEEKS)
1. FIBRINOUS OR DRY PERICARDITIS
2. EFFUSIVE PERICARDITIS
B. SUBACUTE PERICARDITIS (6 WEEKS TO 6 MONTHS)
1. EFFUSIVE
2. CONSTRICTIVE
C. CHRONIC PERICARDITIS (> 6 MONTHS)
1. CONSTRICTIVE
2. EFFUSIVE
3. ADHESIVE
ETIOLOGIC CLASSIFICATION
A. INFECTIOUS PERICARDITIS
1. VIRAL – COXSACKIE B
2. TUBERCULOUS
3. PYOGENIC
4. MYOCOTIC
5. OTHER INFECTIONS (SYPHILITIC, PARASITIC)
B. NON-INFECTIOUS PERICARDITIS
1. ACUTE MYOCARDIAL INFARCTION
2. URAEMIA
3. NEOPLASIA
A.PRIMARY TUMOR ( BENIGN OR MALIGNANT)
B. TUMORS METASTATIC TO PERICARDIUM
4. MYXOEDEMA
5. CHOLESTEROL
6. CHYLOPERICARDIUM
7. TRAUMA
A. PENETRATING CHEST WALL
B. NON – PENETRATING
8. AORTIC ANEURYSM (WITH LEAKAGE INTO PERICARDIAL SAC)
9. POST- RADIATION
10. FAMILIAL MEDITERANEAN FEVER
11. FAMILIAL PERICARDITIS
12. SARCOIDOSIS
13. ACUTE IDIOPATHIC
C. PERICARDITIS PRESUMABLY RELATED TO HYPERSENSITIVITY OR AUTO- IMMUNITY RHEUMATIC FEVER
COLLAGEN VASCULAR DISEASE
A. SYSTEMIC LUPUS ERYTHEMATOSUS
B. RHEUMATOID ARTHRITIS
C. SCLERODERMA
DRUG – INDUCED
A. PROCAINAMIDE
B. HYDRALAZINE
C. OTHER
POST CARDIAC INJURY
A. POST MYOCARDIAL INFARCTION (DRESSLER’S SYNDROME)
B. POST-PERICARDIOTOMY
ACUTE PERICARDITIS
COMMON CAUSES
MYOCARDIAL INFARCTION
VIRAL INFECTIONS – COXACKIE B VIRUS
TUBERCULOSIS
RHEUMATIC FEVER
URAEMIA
MALIGNANCY
CONNECTIVE TISSUE DISORDERS-SLE
POST PERICARDIOTOMY
POST RADIATION
SYMPTOMS
CHEST PAIN
•PRECARDIAL, SHARP
•REFERED TO THE NECK OR SHOULDER
•RELIEVED BY SITTING FORWARD , MADE WORSE BY LYING DOWN, MOVEMENT, RESPIRATION AND SWALLOWING
SIGNS
PERICARDIAL FRICTION RUB
•DIAGNOSTIC
•SUPERFICIAL, SCRATCHING, LEATHERY - HAVING “TO AND FRO” CHARACTER
•BEST HEARD TO THE LEFT OF THE LOWER STERNUM.
INVESTIGATIONS
•ECG
ST ELEVATION WITH CONCAVITY UPWARDS IN AL THE LEADS FACING EPICARDIAL SURFACE.
LATER ST SEGMENT FALLS AND T- WAVE INVERSION OCCURS WHICH BECOMES NORMAL WITH RECOVERY
•DETECTION OF THE UNDERLYING CAUSE
MYOCARDIAL INFRACTION, VIRAL ANTIBODIES, TUBERCULOSIS, CT DISORDERS, URAEMIA, RHEUMATIC FEVER.
TREATMENT
•BED REST
•NSAIDS – ASPRIN, INDOMETHACIN
•STEROIDS IN SEVERE CASES
•TREATMENT OF THE UNDERLYING DISEASE
PURULENT – ANTIBIOTICS, PARACENTESIS,
MAY BE SURGICAL DRAINAGE
TUBERCULOUS – ANTITUBERCULOUS DRUGS
C.T. DISORDER – STEROIDS
PERICARDIAL EFFUSION
ØACCUMULATION OF FLUID IN THE PERICARDIAL SAC MAY ACCOMPANY ACUTE PERICARDITIS OR MAY OCCUR AS A CHRONIC CONDITION.
ØALMOST ALL THE AETIOLOGIES OF ACUTE PERICARDITIS MAY INDUCE THE FORMATION OF PERICARDIAL EFFUSION.
ØTHE SPEED OF ACCUMULATION OF FLUID IN THE PERICARDIUM IS IMPORTANT IN DETERMINING THE INTRA – PERICARDIAL PRESSURE.
ØWHEN THE ACCUMULATION IS SLOW, THE PERICARDIUM DISTENDS GRADUALLY AND THE INTRA – PERICARDIAL PRESSURE DOES NOT RISE MUCH EVEN IN THE PRESENCE OF A MASSIVE EFFUSION
ØWHEN THE FLUID ACCUMULATES RAPIDLY OR IS LARGER THAN THE CPACITY OF THE PERICADIAL SAC, THE INTRA – PERICARDIAL PRESSURE WILL RISE, CAUSING MECHANICAL COMPRESSION OF THE HEART AND PREVENTING VENTRICULAR FILLING RESULTING IN FALL OF CARDIAC OUTPUT- CARDIAC TEMPONADE
CLINICAL FEATURES
SYMPTOMS - NOT VERY MARKED:
ØPAIN OF PERICARDITIS MAY BE REPLACED BY SENSE OF PRECARDIAL OPPRESSION USUALLY WITH BREATHLESSNESS AS THE EFFUSION DEVELOPS.
ØSYMPTOMS DUE TO UNDERLYING CAUSE
SIGNS - VERY MARKED
ØRAISED JVP WITH OTHER SIGNS OF SYST. VENOUS HT
ØPULSUS PARADOXUS - PULSE VOLUME AND B.P FALLS DURING INSPIRATION
ØFRIEDREICH’S SIGN: SHARP DIASTOLIC COLLAPSE OF JVP
ØKUSSMAUL’S SIGN: INCREASED IN JVP DURING
INSPIRATION-VENOUS PULSUS PARADOXUS
APICAL IMPULSE MAY NOT BE PALPABLE, AREA OF CARDIAC DULLNESS MAY BE INCREASED AND HT. SOUNDS ARE SOFT
ØPERICARDIAL FRICTION RUB MAY BE AUDIBLE BUT DISAPPEARS AS THE FLUID SEPARATES THE VISCERAL AND PARIETAL LAYERS
ØSIGNS OF REDUCED CARDIAC OUTPUT MAY BE PRESENT
CARDIAC TAMPONADE
ØCOMPRESSION OF THE HEART BY A LARGE OR RAPIDLY DEVELOPING EFFUSION WHICH INTERFERES WITH DIASTOLIC FILLING OF THE HEART AND PRODUCES SEVERE MECHANICAL EMBARRASSMENT OF THE CIRCULATION; RESULTING IN FALL OF CARDIAC OUTPUT.
ØTHE JVP IS VERY HIGH, PULSUS PARADOXUS IS MARKED, URINARY OUTPUT FALLS AND CLINICAL PICTURE OF ACUTE CIRCULATORY FAILURE MAY DEVELOP.
ØPULMONARY OEDEMA USUALLY DOES NOT DEVELOP.
INVESTIGATIONS
ØX-RAY CHEST: INCREASINGLY LARGE, GLOBULAR HEART WITH SHARP OUTLINES AND RELATIVELY DRY LUNG FIELDS.
ØECG :SMALL COMPLEXES, TACHYCARDIA, Electrical alternans is pathognomonic- due to the heart swinging within the large effusion
ØECHOCARDIOGRAPHY : THE MOST USEFUL TEST TO DIAGNOSE PERICARDIAL EFFUSION BY SHOWING ECHO-FREE ZONE BETWEEN THE POSTERIOR WALL OF THE L. VENTRICLE AND THE PERICARDIUM.
ØCT SCAN / MRI
ØPERICARDIAL FLUID ANALYSIS
ØPERICARDIAL BIOPSY
TREATMENT
1.PERICARDIOCENTESIS
vDIAGNOSTIC
vTHERAPEUTIC
- XIPHISTERNAL APPROACH
- APICAL APPROACH
vFOR CONTINUOUS DRAINAGE, PLASTIC CANNULA MAY BE LIFT IN PLACE
2. PERICARDIAL FENESTRATION : SUGICAL CREATION OF A WINDOW IN THE PERICARDIUM WHEN FLUID ACCUMULATES REPEATEDLY.
3. SPECIFIC THERAPY :
v ANTIBIOTICS IN PYOGENIC FLUID
vANTITUBERCULOUS DRUGS IN TUBERCULOUS EFFUSION.
vSTEROIDS : SLE, AUTOIMUNE DISORDERS,OCCASIONALLY USED TO PREVENT
THE DEVELOPMENT OF CONSTRICTIVE PERICARDITIS
CONSTRICTIVE PERICARDITIS
FOLLOWING TUBERCULOUS PERICARDIAL EFFUSION,
HAEMOPERICARDIUM, PYOGENIC PERICRDITIS OR
ACUTE PERICARDITIS DUE TO VIRAL INFECTION AND
POST RADIATION PERICARDITIS, THE
PERICARDIUM MAY BECOME THICK, FIBROUS AND
ULTIMATELY CALCIFIED AND RIGID.
THE HEART IS THEN ENCASED IN A RIGID SHELL AND
CANNOT EXPAND AND FILL IN DIASTOLE.
CLINICAL FEATURES
Ø BREATHLESSNESS IS NOT PROMINENT AS THERE IS NOT MUCH PULMONARY CONGESTION
ØSIGNS OF SYSTEMIC VENOUS HYPERTENSION -
RAISED JVP, HEPATOMEGALLY, ASCITES AND DEPENDENT OEDEMA
ØSIGNS OF IMPAIRED V. FILLING
KUSSMAUL’S SIGN, PULSUS PARADOXUS AND FRIEDRIECH’S SIGN
ØATRIAL FIBRILLATION IS COMMON
ØPERICARDIAL KNOCK – A LOUD EARLY THIRD HEART SOUND
ØTHE APICAL IMPULSE IS NOT FORCEFUL AND HEART SOUNDS ARE QUIET- “SMALL QUIET HEART”.
INVESTIGATIONS
ØX-RAY CHEST
RELATIVELY SMALL HEART WITH SHAGGY HEART BORDERS AND PERICARDIAL CALCIFICATION ON THE LATERAL FILM
Ø ECG
LOW QRS COMPLEXES AND INVERTED T – WAVES.
Ø ECHOCRDIOGRAM
THICKENED PERICARDIUM, RELATIVE IMMOBILITY OF THE
HEART WALLS.
Ø CT SCAN / MRI SCAN
THICKENED PERICARDIUM, CALCIFICATION
TREATMENT
ØPERICARDIECTOMY
SURGICAL RESECTION OF PERICARDIUM PRODUCES RAPID IMPROVEMENT
Q1. WHAT IS THE MOST LIKELY CLINICAL DIAGNOSIS
Q2. WHAT IS THE MOST LIKELY ETILOGICAL
DIAGNOSIS
Q3. WHAT WILL BE THE MOST HELPFUL IMEDIATE
INVESTIGATION
DISEASES OF PERICARDIUM
NORMAL PERICARDIUM
ØLUBRICATES THE SURFACE OF THE HEART
ØPREVENTS SUDDEN DEFORMATION OF THE HEART
ØACTS AS A BARRIER TO THE SPREAD OF INFECTION
ØPREVENTS DISLOCATION OF THE HEART
CLINICAL PRESENTATION OF PERICARDIAL DISEASE
1.ACUTE PERICARDITIS
2. PERICARDIAL EFFUSION
3. CONSTRICTIVE PERICARDITIS
CLASSIFICATION OF PERICARDITIS
•CLINICAL CLASSIFICATION
A. ACUTE PERICARDITIS (< 6 WEEKS)
1. FIBRINOUS OR DRY PERICARDITIS
2. EFFUSIVE PERICARDITIS
B. SUBACUTE PERICARDITIS (6 WEEKS TO 6 MONTHS)
1. EFFUSIVE
2. CONSTRICTIVE
C. CHRONIC PERICARDITIS (> 6 MONTHS)
1. CONSTRICTIVE
2. EFFUSIVE
3. ADHESIVE
ETIOLOGIC CLASSIFICATION
A. INFECTIOUS PERICARDITIS
1. VIRAL – COXSACKIE B
2. TUBERCULOUS
3. PYOGENIC
4. MYOCOTIC
5. OTHER INFECTIONS (SYPHILITIC, PARASITIC)
B. NON-INFECTIOUS PERICARDITIS
1. ACUTE MYOCARDIAL INFARCTION
2. URAEMIA
3. NEOPLASIA
A.PRIMARY TUMOR ( BENIGN OR MALIGNANT)
B. TUMORS METASTATIC TO PERICARDIUM
4. MYXOEDEMA
5. CHOLESTEROL
6. CHYLOPERICARDIUM
7. TRAUMA
A. PENETRATING CHEST WALL
B. NON – PENETRATING
8. AORTIC ANEURYSM (WITH LEAKAGE INTO PERICARDIAL SAC)
9. POST- RADIATION
10. FAMILIAL MEDITERANEAN FEVER
11. FAMILIAL PERICARDITIS
12. SARCOIDOSIS
13. ACUTE IDIOPATHIC
C. PERICARDITIS PRESUMABLY RELATED TO HYPERSENSITIVITY OR AUTO- IMMUNITY RHEUMATIC FEVER
COLLAGEN VASCULAR DISEASE
A. SYSTEMIC LUPUS ERYTHEMATOSUS
B. RHEUMATOID ARTHRITIS
C. SCLERODERMA
DRUG – INDUCED
A. PROCAINAMIDE
B. HYDRALAZINE
C. OTHER
POST CARDIAC INJURY
A. POST MYOCARDIAL INFARCTION (DRESSLER’S SYNDROME)
B. POST-PERICARDIOTOMY
ACUTE PERICARDITIS
COMMON CAUSES
MYOCARDIAL INFARCTION
VIRAL INFECTIONS – COXACKIE B VIRUS
TUBERCULOSIS
RHEUMATIC FEVER
URAEMIA
MALIGNANCY
CONNECTIVE TISSUE DISORDERS-SLE
POST PERICARDIOTOMY
POST RADIATION
SYMPTOMS
CHEST PAIN
•PRECARDIAL, SHARP
•REFERED TO THE NECK OR SHOULDER
•RELIEVED BY SITTING FORWARD , MADE WORSE BY LYING DOWN, MOVEMENT, RESPIRATION AND SWALLOWING
SIGNS
PERICARDIAL FRICTION RUB
•DIAGNOSTIC
•SUPERFICIAL, SCRATCHING, LEATHERY - HAVING “TO AND FRO” CHARACTER
•BEST HEARD TO THE LEFT OF THE LOWER STERNUM.
INVESTIGATIONS
•ECG
ST ELEVATION WITH CONCAVITY UPWARDS IN AL THE LEADS FACING EPICARDIAL SURFACE.
LATER ST SEGMENT FALLS AND T- WAVE INVERSION OCCURS WHICH BECOMES NORMAL WITH RECOVERY
•DETECTION OF THE UNDERLYING CAUSE
MYOCARDIAL INFRACTION, VIRAL ANTIBODIES, TUBERCULOSIS, CT DISORDERS, URAEMIA, RHEUMATIC FEVER.
TREATMENT
•BED REST
•NSAIDS – ASPRIN, INDOMETHACIN
•STEROIDS IN SEVERE CASES
•TREATMENT OF THE UNDERLYING DISEASE
PURULENT – ANTIBIOTICS, PARACENTESIS,
MAY BE SURGICAL DRAINAGE
TUBERCULOUS – ANTITUBERCULOUS DRUGS
C.T. DISORDER – STEROIDS
PERICARDIAL EFFUSION
ØACCUMULATION OF FLUID IN THE PERICARDIAL SAC MAY ACCOMPANY ACUTE PERICARDITIS OR MAY OCCUR AS A CHRONIC CONDITION.
ØALMOST ALL THE AETIOLOGIES OF ACUTE PERICARDITIS MAY INDUCE THE FORMATION OF PERICARDIAL EFFUSION.
ØTHE SPEED OF ACCUMULATION OF FLUID IN THE PERICARDIUM IS IMPORTANT IN DETERMINING THE INTRA – PERICARDIAL PRESSURE.
ØWHEN THE ACCUMULATION IS SLOW, THE PERICARDIUM DISTENDS GRADUALLY AND THE INTRA – PERICARDIAL PRESSURE DOES NOT RISE MUCH EVEN IN THE PRESENCE OF A MASSIVE EFFUSION
ØWHEN THE FLUID ACCUMULATES RAPIDLY OR IS LARGER THAN THE CPACITY OF THE PERICADIAL SAC, THE INTRA – PERICARDIAL PRESSURE WILL RISE, CAUSING MECHANICAL COMPRESSION OF THE HEART AND PREVENTING VENTRICULAR FILLING RESULTING IN FALL OF CARDIAC OUTPUT- CARDIAC TEMPONADE
CLINICAL FEATURES
SYMPTOMS - NOT VERY MARKED:
ØPAIN OF PERICARDITIS MAY BE REPLACED BY SENSE OF PRECARDIAL OPPRESSION USUALLY WITH BREATHLESSNESS AS THE EFFUSION DEVELOPS.
ØSYMPTOMS DUE TO UNDERLYING CAUSE
SIGNS - VERY MARKED
ØRAISED JVP WITH OTHER SIGNS OF SYST. VENOUS HT
ØPULSUS PARADOXUS - PULSE VOLUME AND B.P FALLS DURING INSPIRATION
ØFRIEDREICH’S SIGN: SHARP DIASTOLIC COLLAPSE OF JVP
ØKUSSMAUL’S SIGN: INCREASED IN JVP DURING
INSPIRATION-VENOUS PULSUS PARADOXUS
APICAL IMPULSE MAY NOT BE PALPABLE, AREA OF CARDIAC DULLNESS MAY BE INCREASED AND HT. SOUNDS ARE SOFT
ØPERICARDIAL FRICTION RUB MAY BE AUDIBLE BUT DISAPPEARS AS THE FLUID SEPARATES THE VISCERAL AND PARIETAL LAYERS
ØSIGNS OF REDUCED CARDIAC OUTPUT MAY BE PRESENT
CARDIAC TAMPONADE
ØCOMPRESSION OF THE HEART BY A LARGE OR RAPIDLY DEVELOPING EFFUSION WHICH INTERFERES WITH DIASTOLIC FILLING OF THE HEART AND PRODUCES SEVERE MECHANICAL EMBARRASSMENT OF THE CIRCULATION; RESULTING IN FALL OF CARDIAC OUTPUT.
ØTHE JVP IS VERY HIGH, PULSUS PARADOXUS IS MARKED, URINARY OUTPUT FALLS AND CLINICAL PICTURE OF ACUTE CIRCULATORY FAILURE MAY DEVELOP.
ØPULMONARY OEDEMA USUALLY DOES NOT DEVELOP.
INVESTIGATIONS
ØX-RAY CHEST: INCREASINGLY LARGE, GLOBULAR HEART WITH SHARP OUTLINES AND RELATIVELY DRY LUNG FIELDS.
ØECG :SMALL COMPLEXES, TACHYCARDIA, Electrical alternans is pathognomonic- due to the heart swinging within the large effusion
ØECHOCARDIOGRAPHY : THE MOST USEFUL TEST TO DIAGNOSE PERICARDIAL EFFUSION BY SHOWING ECHO-FREE ZONE BETWEEN THE POSTERIOR WALL OF THE L. VENTRICLE AND THE PERICARDIUM.
ØCT SCAN / MRI
ØPERICARDIAL FLUID ANALYSIS
ØPERICARDIAL BIOPSY
TREATMENT
1.PERICARDIOCENTESIS
vDIAGNOSTIC
vTHERAPEUTIC
- XIPHISTERNAL APPROACH
- APICAL APPROACH
vFOR CONTINUOUS DRAINAGE, PLASTIC CANNULA MAY BE LIFT IN PLACE
2. PERICARDIAL FENESTRATION : SUGICAL CREATION OF A WINDOW IN THE PERICARDIUM WHEN FLUID ACCUMULATES REPEATEDLY.
3. SPECIFIC THERAPY :
v ANTIBIOTICS IN PYOGENIC FLUID
vANTITUBERCULOUS DRUGS IN TUBERCULOUS EFFUSION.
vSTEROIDS : SLE, AUTOIMUNE DISORDERS,OCCASIONALLY USED TO PREVENT
THE DEVELOPMENT OF CONSTRICTIVE PERICARDITIS
CONSTRICTIVE PERICARDITIS
FOLLOWING TUBERCULOUS PERICARDIAL EFFUSION,
HAEMOPERICARDIUM, PYOGENIC PERICRDITIS OR
ACUTE PERICARDITIS DUE TO VIRAL INFECTION AND
POST RADIATION PERICARDITIS, THE
PERICARDIUM MAY BECOME THICK, FIBROUS AND
ULTIMATELY CALCIFIED AND RIGID.
THE HEART IS THEN ENCASED IN A RIGID SHELL AND
CANNOT EXPAND AND FILL IN DIASTOLE.
CLINICAL FEATURES
Ø BREATHLESSNESS IS NOT PROMINENT AS THERE IS NOT MUCH PULMONARY CONGESTION
ØSIGNS OF SYSTEMIC VENOUS HYPERTENSION -
RAISED JVP, HEPATOMEGALLY, ASCITES AND DEPENDENT OEDEMA
ØSIGNS OF IMPAIRED V. FILLING
KUSSMAUL’S SIGN, PULSUS PARADOXUS AND FRIEDRIECH’S SIGN
ØATRIAL FIBRILLATION IS COMMON
ØPERICARDIAL KNOCK – A LOUD EARLY THIRD HEART SOUND
ØTHE APICAL IMPULSE IS NOT FORCEFUL AND HEART SOUNDS ARE QUIET- “SMALL QUIET HEART”.
INVESTIGATIONS
ØX-RAY CHEST
RELATIVELY SMALL HEART WITH SHAGGY HEART BORDERS AND PERICARDIAL CALCIFICATION ON THE LATERAL FILM
Ø ECG
LOW QRS COMPLEXES AND INVERTED T – WAVES.
Ø ECHOCRDIOGRAM
THICKENED PERICARDIUM, RELATIVE IMMOBILITY OF THE
HEART WALLS.
Ø CT SCAN / MRI SCAN
THICKENED PERICARDIUM, CALCIFICATION
TREATMENT
ØPERICARDIECTOMY
SURGICAL RESECTION OF PERICARDIUM PRODUCES RAPID IMPROVEMENT
Management of Upper GI bleed, by Dr. Hashim uddin
Assessment of Upper GI Bleeding.
DR HASHIM UDDIN AZAM
Upper GI Bleeding
• Haemorrhage from the GI Tract and adnexal structures proximal to the Duodenal-Jejunal flexure.
Upper GI Bleeds
v Difficult to assess incidence/prevalence.
v 100 episodes/100 000 people per year US
v (Silverstein et al 1981)
v Represents initial Sx of GI disease in >30% of patients (Fischer et al 1999).
v ~50% of cases develop during hospitalization*.
v Associated with significant Morbidity.
v Mortality 5-12% (mostly cardiovascular)
v Higher in rebleed patients (30-40%)
v (Friedman 1993)
Acute vs Chronic Bleeds
•Acute
–Present via Acute referral pathway.
–Presentation
Bleeding
Degree of shock due to blood/volume loss.
May have other GI symptomatology.
•Chronic
–Present to GP (ED)
–Presentation
Related to chronic anaemia. May report Bleed.
Other Sx of GI pathology.
Incidental finding.
No degree of shock.
•Haematemesis
–Emesis of blood containing fluid.
•Fresh or Altered (Coffee ground)
•Melaena
–Passage of Altered Blood Stool
•Black, Tarry, Offensive Stool
•Indicates Bleed proximal to …
•Haematochezia
–Passage of fresh blood and clots per rectum.
Causes
•Oesophageal
•Varices (5-10%), Oesophagitis reflux or other, Malignancy, Mallory Weiss Tear, rupture.
•Gastric
•Gastritis, Peptic ulcer(70-80%), Malignancy, Dieulafoy.
•Duodenal
•Ulcer, Aorto-enteric fistula, Diverticulum.
•Adnexal
•Haematobilia.
Initial Clinical Assessment
•Rapid History
–? Symptomatic Shock
–Bleeding history
–Other features of GI pathology
–Co-Morbidities
•Bleeding Diathesis
•Liver/renal failure
•Cardiac disease
•Recent medications.
•Examination
–Volume Status
–Gastrointestinal examination
–Examination of Vomitus/Melaena
–Re-examine Volume status
•Degree of Shock
Initial Management
•Investigations
•FBE, Coags, G+M
•U+E, LFT, Amylase/Lipase
•Initial Resuscitation
•Aggressive IV Fluids
•Appropriate Monitoring
•?Empirical PPI
What Next?
Nasogastric aspirate/lavage.
Endoscopy
Oral contrast radiology
Angiography
1--?Nasogastric Aspirate/Lavage
•Roles
–Distinguish Upper from Lower GI Bleeds
•Non-Bloody aspirate seen in up to 16% of UGIB
–Clear stomach for Endoscopy
–Assist haemostatis (lavage)
•No Evidence to support this. (tepid or chilled)
?Nasogastric Aspirate/Lavage
•Roles
–? Bleeding at presentation
•Initial aspirate 79% sensitivity, If positive 53% specificity.
–Monitor for rebleed (ongoing lavage)
•Most sensitive “online” marker for this.
–Prognostics
•Clear aspirate 6% mortality, Bloody 18% mortality
2--Endoscopy-why
•Availability
•Diagnostic Efficacy
•Low associated morbidity (0.01-0.05%)
•Therapeutic manoevres
•Sclerosant injection
•Electro/photocoagulation
•Banding
•Affords prognostic information.
Endoscopy-why
•Endoscopic Diagnosis
–Inspection
•Mucosa and its pathology
•Active bleeding sources
•Stigmata of Recent Haemorrhage
–Old blood, adherent clot etc.
•Varices-If not bleeding and no SRH-variceal bleed becomes a diagnosis of exclusion.
–Diagnostic testing
•Allows Biopsy, HP testing
•Diagnostic Efficacy
–Identifies bleeding site in 70-96% with near 0 false positive rate.
–Differentiates major pathologies in >90%
Endoscopy-when
•Ideally
–Bleeding ceased.
–Patient stable.
–SRH still present.
–No delay during which rebleeding (10-30%) may occur.
–(Lieberman 1993, Laine 1998).
•Sooner rather than later
–Really?
•Spiegel et al 2001 reviewed data from 23 studies
–Most had failings
–Early endoscopy safe, despite earlier reports.
–No decrease in mortality but decrease in transfusion and length of stay.
–Recommended prospective trial.
•Practically
–Small Bleed (1-2u) now ceased.
•Elective Endoscopy
–Large bleed (Non-Variceal) now ceased.
•Urgent when stable
–Suspected Variceal Bleed.
•Urgent
–Ongoing or recurrent bleeding.
•Urgent
–(Lieberman 1993)
Endoscopy-other issues
•Contra-indications
•AMI, Acute Abdomen
•Refusal, unco-operative.
•Patients in extremis
•May require intubation prior to endoscopy.
3--Oral Contrast Radiology
•Limited diagnostic capacity.
–Sensitivity 70-80%, false positive 10-20%
•Can interfere with subsequent testing.
•No prognostic information.
•Poor regional availability.
Endoscopy vs Contrast Radiography
•Early reports
–No benefit of endoscopy over radiography in terms of mortality, rebleeding, admission length or transfusion requirements
–Peterson et al 1981
“the development of therapeutic methods that are better than empiric antacid therapy for specific lesions may demand modofocation of our conclusions”
Angiography
•Rarely used
–endoscopy too successful.
•Localises bleeding points.
–Relies on extravasation not pathology.
•Poor results for varices.
•Therapeutic potential-
–vasopressin infusion or embolisation.
•Requires bleed rate of >0.5-1.0ml/min for positive result.
4--Angiography
•Indications
–Non-diagnostic Endoscopy
–Bleed too fast to safely ‘scope.
•Can localise bleeding point in ~75% of cases.
–Failed endoscopic therapy and need to avoid surgery.
•IA Vasopressin-60-90% successful in stopping gastric bleeds.
•Embolisation (coils, PVA)-~80% success.
Upper GI Bleed prognostics.
•Predictable outcomes
–Need for treatment.
–Risk of Re-bleed.
–Risk of Death
•Determines management.
–Outpatient vs Inpatient
–Ward vs HDU vs ICU
–Timing of endoscopy
–? Angiography
–Length of stay
–
Need for Treatment
•Blatchford et al 2000
–Developed a scoring system:
•predicts need for intervention Endoscopy, transfusion etc.
•Input data consists of clinical findings and laboratory results.
•Small trial-not yet validated
Risk of Rebleed.
•Ulcers
–Dependant on Ulcer appearance (Schaefer, Lieberman)
•Actively bleeding 80% chance on ongoing/recurrent bleed.
•Fibrin clot on visible vessel 40%
•Adherent clot 20%
•Flat pigmented spot in crater 10%
•Clear white base ~5%
Mortality Risk
•Extensive writings have been published on this point.
–Collated by Hussain et al 2000
–Predictors of mortality
Ø Host
o Age>60 yrs, Signif co-morbidities, raised INR, NSAIDs
Ø Patient course
o Transfusion >5 units, Shock, LFT changes, Renal failure.
Ø Endoscopic factors
o Varices, Active bleeding, SRH, Ulcer site.
The Friendly Version.
•Scoring systems
–Several described, few validated.
–Rockall et al 1996
•Analysed 4185 cases, prospective data collection.
•Devised numerical scoring system that predicts rebleeding and mortality risk.
•Validated on >1600 cases originally.
•Subsequently validated in US, Holland.
Rockall Scoring System.
•Rebleed risk
–Score 0-2 5%; 3-5 10-25%; 6-8+ 33-45%
•Mortality risk
–Score 0-2 0%; 3-5 3-10%; 6-8+ 17-40%
Conclusion
•Its trickier than you thought.
•Clinical assessment is important particularly in guiding resuscitation.
•Endoscopy (early) is now the cornerstone of diagnosis.
•Endoscopy also yields prognostic information that may guide clinical decisions.
DR HASHIM UDDIN AZAM
Upper GI Bleeding
• Haemorrhage from the GI Tract and adnexal structures proximal to the Duodenal-Jejunal flexure.
Upper GI Bleeds
v Difficult to assess incidence/prevalence.
v 100 episodes/100 000 people per year US
v (Silverstein et al 1981)
v Represents initial Sx of GI disease in >30% of patients (Fischer et al 1999).
v ~50% of cases develop during hospitalization*.
v Associated with significant Morbidity.
v Mortality 5-12% (mostly cardiovascular)
v Higher in rebleed patients (30-40%)
v (Friedman 1993)
Acute vs Chronic Bleeds
•Acute
–Present via Acute referral pathway.
–Presentation
Bleeding
Degree of shock due to blood/volume loss.
May have other GI symptomatology.
•Chronic
–Present to GP (ED)
–Presentation
Related to chronic anaemia. May report Bleed.
Other Sx of GI pathology.
Incidental finding.
No degree of shock.
•Haematemesis
–Emesis of blood containing fluid.
•Fresh or Altered (Coffee ground)
•Melaena
–Passage of Altered Blood Stool
•Black, Tarry, Offensive Stool
•Indicates Bleed proximal to …
•Haematochezia
–Passage of fresh blood and clots per rectum.
Causes
•Oesophageal
•Varices (5-10%), Oesophagitis reflux or other, Malignancy, Mallory Weiss Tear, rupture.
•Gastric
•Gastritis, Peptic ulcer(70-80%), Malignancy, Dieulafoy.
•Duodenal
•Ulcer, Aorto-enteric fistula, Diverticulum.
•Adnexal
•Haematobilia.
Initial Clinical Assessment
•Rapid History
–? Symptomatic Shock
–Bleeding history
–Other features of GI pathology
–Co-Morbidities
•Bleeding Diathesis
•Liver/renal failure
•Cardiac disease
•Recent medications.
•Examination
–Volume Status
–Gastrointestinal examination
–Examination of Vomitus/Melaena
–Re-examine Volume status
•Degree of Shock
Initial Management
•Investigations
•FBE, Coags, G+M
•U+E, LFT, Amylase/Lipase
•Initial Resuscitation
•Aggressive IV Fluids
•Appropriate Monitoring
•?Empirical PPI
What Next?
Nasogastric aspirate/lavage.
Endoscopy
Oral contrast radiology
Angiography
1--?Nasogastric Aspirate/Lavage
•Roles
–Distinguish Upper from Lower GI Bleeds
•Non-Bloody aspirate seen in up to 16% of UGIB
–Clear stomach for Endoscopy
–Assist haemostatis (lavage)
•No Evidence to support this. (tepid or chilled)
?Nasogastric Aspirate/Lavage
•Roles
–? Bleeding at presentation
•Initial aspirate 79% sensitivity, If positive 53% specificity.
–Monitor for rebleed (ongoing lavage)
•Most sensitive “online” marker for this.
–Prognostics
•Clear aspirate 6% mortality, Bloody 18% mortality
2--Endoscopy-why
•Availability
•Diagnostic Efficacy
•Low associated morbidity (0.01-0.05%)
•Therapeutic manoevres
•Sclerosant injection
•Electro/photocoagulation
•Banding
•Affords prognostic information.
Endoscopy-why
•Endoscopic Diagnosis
–Inspection
•Mucosa and its pathology
•Active bleeding sources
•Stigmata of Recent Haemorrhage
–Old blood, adherent clot etc.
•Varices-If not bleeding and no SRH-variceal bleed becomes a diagnosis of exclusion.
–Diagnostic testing
•Allows Biopsy, HP testing
•Diagnostic Efficacy
–Identifies bleeding site in 70-96% with near 0 false positive rate.
–Differentiates major pathologies in >90%
Endoscopy-when
•Ideally
–Bleeding ceased.
–Patient stable.
–SRH still present.
–No delay during which rebleeding (10-30%) may occur.
–(Lieberman 1993, Laine 1998).
•Sooner rather than later
–Really?
•Spiegel et al 2001 reviewed data from 23 studies
–Most had failings
–Early endoscopy safe, despite earlier reports.
–No decrease in mortality but decrease in transfusion and length of stay.
–Recommended prospective trial.
•Practically
–Small Bleed (1-2u) now ceased.
•Elective Endoscopy
–Large bleed (Non-Variceal) now ceased.
•Urgent when stable
–Suspected Variceal Bleed.
•Urgent
–Ongoing or recurrent bleeding.
•Urgent
–(Lieberman 1993)
Endoscopy-other issues
•Contra-indications
•AMI, Acute Abdomen
•Refusal, unco-operative.
•Patients in extremis
•May require intubation prior to endoscopy.
3--Oral Contrast Radiology
•Limited diagnostic capacity.
–Sensitivity 70-80%, false positive 10-20%
•Can interfere with subsequent testing.
•No prognostic information.
•Poor regional availability.
Endoscopy vs Contrast Radiography
•Early reports
–No benefit of endoscopy over radiography in terms of mortality, rebleeding, admission length or transfusion requirements
–Peterson et al 1981
“the development of therapeutic methods that are better than empiric antacid therapy for specific lesions may demand modofocation of our conclusions”
Angiography
•Rarely used
–endoscopy too successful.
•Localises bleeding points.
–Relies on extravasation not pathology.
•Poor results for varices.
•Therapeutic potential-
–vasopressin infusion or embolisation.
•Requires bleed rate of >0.5-1.0ml/min for positive result.
4--Angiography
•Indications
–Non-diagnostic Endoscopy
–Bleed too fast to safely ‘scope.
•Can localise bleeding point in ~75% of cases.
–Failed endoscopic therapy and need to avoid surgery.
•IA Vasopressin-60-90% successful in stopping gastric bleeds.
•Embolisation (coils, PVA)-~80% success.
Upper GI Bleed prognostics.
•Predictable outcomes
–Need for treatment.
–Risk of Re-bleed.
–Risk of Death
•Determines management.
–Outpatient vs Inpatient
–Ward vs HDU vs ICU
–Timing of endoscopy
–? Angiography
–Length of stay
–
Need for Treatment
•Blatchford et al 2000
–Developed a scoring system:
•predicts need for intervention Endoscopy, transfusion etc.
•Input data consists of clinical findings and laboratory results.
•Small trial-not yet validated
Risk of Rebleed.
•Ulcers
–Dependant on Ulcer appearance (Schaefer, Lieberman)
•Actively bleeding 80% chance on ongoing/recurrent bleed.
•Fibrin clot on visible vessel 40%
•Adherent clot 20%
•Flat pigmented spot in crater 10%
•Clear white base ~5%
Mortality Risk
•Extensive writings have been published on this point.
–Collated by Hussain et al 2000
–Predictors of mortality
Ø Host
o Age>60 yrs, Signif co-morbidities, raised INR, NSAIDs
Ø Patient course
o Transfusion >5 units, Shock, LFT changes, Renal failure.
Ø Endoscopic factors
o Varices, Active bleeding, SRH, Ulcer site.
The Friendly Version.
•Scoring systems
–Several described, few validated.
–Rockall et al 1996
•Analysed 4185 cases, prospective data collection.
•Devised numerical scoring system that predicts rebleeding and mortality risk.
•Validated on >1600 cases originally.
•Subsequently validated in US, Holland.
Rockall Scoring System.
•Rebleed risk
–Score 0-2 5%; 3-5 10-25%; 6-8+ 33-45%
•Mortality risk
–Score 0-2 0%; 3-5 3-10%; 6-8+ 17-40%
Conclusion
•Its trickier than you thought.
•Clinical assessment is important particularly in guiding resuscitation.
•Endoscopy (early) is now the cornerstone of diagnosis.
•Endoscopy also yields prognostic information that may guide clinical decisions.
JNC 7 Report on High Blood Pressure
The JNC 7 Report By Dr. Sultan Mehmood
nThe Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure
Accurate BP Measurement in the Office
1. The Auscultatory method of BP measurement with a properly calibrated and validated instrument should be used.
2. Patients should be seated quietly for at least 5 minutes in a chair rather than on an examination table, with feet on the floor and arms supported at heart level.
3. Measurement of BP in the standing position is indicated periodically, especially in those at risk of postural hypotension.
1. An appropriate sized cuff (cuff bladder encircling at least 80 % of the arm) should be used to ensure accuracy.
2. At least 2 measurements should be made.
3. Systolic BP is the point at which the 1st of two or more sounds is heard (phase 1) and diastolic BP is the point before the disappearance of sounds (phase 5).
n"The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure" provides new guidelines for hypertension prevention and management.
nThe following are the key messages
TABLE:
BP
Classification
Systolic BP
(mmHg)
Diastolic BP (mmHg)
Lifestyle Modification
Without Compelling Indication
With Compelling Indication
Normal
<120
and
<80
Encourage
Prehypertension
120-139
or
80-89
Yes
No Antihypertensive drug indicated
Drugs for the compelling indications (*1)
Stage 1 hypertension
140-159
or
90-99
Yes
Thiazide-type diuretics for most; may consider ACE-inhibitor, ARB, B-blockers, CCB, or combination
Drugs for the compelling indications
Other Antihypertensive drugs (diuretics, ACE inhibitors, ARB, B-blockers, CCB) as needed
Stage 2 hypertension
>160
or
>100
Yes
2-Drugs combination for most (usually thiazide-type diuretic and ACE inhibitors or ARB or B-blockers or CCB) (*2)
Drugs for the compelling indications
Other antihypertensive drugs (diuretics, ACE inhibitors, ARB, B-blockers, CCB) as needed
*1 : Treat patients with chronic kidney disease and diabetes to BP goal of less than 130/80 mmHg
*2 : Initial combined therapy should be used cautiously in those at risk of orthostatic hypotension
n"The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure" provides a new guidelines for hypertension prevention and management.
nThe following are the key messages
I. (1) In persons older than 50 years, systolic blood pressure (BP) of more than 140 mm Hg is a much more important cardiovascular disease (CVD) risk factor than diastolic BP
II. (2) The risk of CVD, beginning at 115/75 mm Hg, doubles with each increment of 20/10 mm Hg;
III. individuals who are normotensive at 55 years of age have a 90% lifetime risk for developing hypertension
IV. (3) Individuals with a systolic BP of 120 to 139 mm Hg or a diastolic BP of 80 to 89 mm Hg should be considered as prehypertensive and require health-promoting lifestyle modifications to prevent CVD
V. (4) Thiazide-type diuretics should be used in drug treatment for most patients with uncomplicated hypertension, either alone or combined with drugs from other classes.
VI. Certain high-risk conditions are compelling indications for the initial use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers,
VII. B-blockers, calcium channel blockers)
VIII. (5) Most patients with hypertension will require 2 or more antihypertensive medications to achieve goal BP (<140/90 mm Hg, or <130/80 mm Hg for patients with diabetes or chronic kidney disease);
IX. (6) If BP is more than 20/10 mm Hg above goal BP, consideration should be given to initiating therapy with 2 agents, 1 of which usually should be a thiazide-type diuretic;
X. (7) The most effective therapy prescribed by the most careful clinician will control hypertension only if patients are motivated.
XI. Motivation improves when patients have positive experiences with and trust in the clinician. Empathy builds trust and is a potent motivator.
XII. Finally, in presenting these guidelines, the committee recognizes that the responsible physician's judgment remains paramount.
LIFESTYLE MODIFICATIONS TO MANAGE HTN
WT. REDUCTION – BMI = 18 – 24
ADOPT DASH (Dietary approaches to stop Hypertention) EATING PLAN : DIET RICH IN FRUITS,VEGS, LOW FAT DIARY PRODUCTS, REDUCED CONTENTS OF SATURATED AND TOTAL FAT
DIETARY SODIUM REDUCTION < 6 G/DAY
PHYSICAL ACTIVITY – 30 MIN/DAY
STOP SMOKING , ALCOHOL
nThe Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure
Accurate BP Measurement in the Office
1. The Auscultatory method of BP measurement with a properly calibrated and validated instrument should be used.
2. Patients should be seated quietly for at least 5 minutes in a chair rather than on an examination table, with feet on the floor and arms supported at heart level.
3. Measurement of BP in the standing position is indicated periodically, especially in those at risk of postural hypotension.
1. An appropriate sized cuff (cuff bladder encircling at least 80 % of the arm) should be used to ensure accuracy.
2. At least 2 measurements should be made.
3. Systolic BP is the point at which the 1st of two or more sounds is heard (phase 1) and diastolic BP is the point before the disappearance of sounds (phase 5).
n"The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure" provides new guidelines for hypertension prevention and management.
nThe following are the key messages
TABLE:
BP
Classification
Systolic BP
(mmHg)
Diastolic BP (mmHg)
Lifestyle Modification
Without Compelling Indication
With Compelling Indication
Normal
<120
and
<80
Encourage
Prehypertension
120-139
or
80-89
Yes
No Antihypertensive drug indicated
Drugs for the compelling indications (*1)
Stage 1 hypertension
140-159
or
90-99
Yes
Thiazide-type diuretics for most; may consider ACE-inhibitor, ARB, B-blockers, CCB, or combination
Drugs for the compelling indications
Other Antihypertensive drugs (diuretics, ACE inhibitors, ARB, B-blockers, CCB) as needed
Stage 2 hypertension
>160
or
>100
Yes
2-Drugs combination for most (usually thiazide-type diuretic and ACE inhibitors or ARB or B-blockers or CCB) (*2)
Drugs for the compelling indications
Other antihypertensive drugs (diuretics, ACE inhibitors, ARB, B-blockers, CCB) as needed
*1 : Treat patients with chronic kidney disease and diabetes to BP goal of less than 130/80 mmHg
*2 : Initial combined therapy should be used cautiously in those at risk of orthostatic hypotension
n"The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure" provides a new guidelines for hypertension prevention and management.
nThe following are the key messages
I. (1) In persons older than 50 years, systolic blood pressure (BP) of more than 140 mm Hg is a much more important cardiovascular disease (CVD) risk factor than diastolic BP
II. (2) The risk of CVD, beginning at 115/75 mm Hg, doubles with each increment of 20/10 mm Hg;
III. individuals who are normotensive at 55 years of age have a 90% lifetime risk for developing hypertension
IV. (3) Individuals with a systolic BP of 120 to 139 mm Hg or a diastolic BP of 80 to 89 mm Hg should be considered as prehypertensive and require health-promoting lifestyle modifications to prevent CVD
V. (4) Thiazide-type diuretics should be used in drug treatment for most patients with uncomplicated hypertension, either alone or combined with drugs from other classes.
VI. Certain high-risk conditions are compelling indications for the initial use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers,
VII. B-blockers, calcium channel blockers)
VIII. (5) Most patients with hypertension will require 2 or more antihypertensive medications to achieve goal BP (<140/90 mm Hg, or <130/80 mm Hg for patients with diabetes or chronic kidney disease);
IX. (6) If BP is more than 20/10 mm Hg above goal BP, consideration should be given to initiating therapy with 2 agents, 1 of which usually should be a thiazide-type diuretic;
X. (7) The most effective therapy prescribed by the most careful clinician will control hypertension only if patients are motivated.
XI. Motivation improves when patients have positive experiences with and trust in the clinician. Empathy builds trust and is a potent motivator.
XII. Finally, in presenting these guidelines, the committee recognizes that the responsible physician's judgment remains paramount.
LIFESTYLE MODIFICATIONS TO MANAGE HTN
WT. REDUCTION – BMI = 18 – 24
ADOPT DASH (Dietary approaches to stop Hypertention) EATING PLAN : DIET RICH IN FRUITS,VEGS, LOW FAT DIARY PRODUCTS, REDUCED CONTENTS OF SATURATED AND TOTAL FAT
DIETARY SODIUM REDUCTION < 6 G/DAY
PHYSICAL ACTIVITY – 30 MIN/DAY
STOP SMOKING , ALCOHOL
Praparing diabetic patient for surgery
PREPARING DIABETIC PATIENT FOR SURGERY
PRE_OP ASSESSMENT
A comprehensive history and physical examination is imporatnt. Since estimates suggest that one third of diabetic patients are unaware of their disease, it may be prudent to screen all patients undergoing intermediate or major surgery by checking glycosylated hemoglobin (HbA1c).
The history should include the following:
Suggestive symptoms (eg, polyuria/polydipsia, blurred vision)
Eating patterns, nutritional status, exercise history, and weight history
Current treatment of diabetes, including medication regimen, diet, and glucose monitoring results
Frequency, severity, and etiology of acute complications (ie, ketoacidosis, hypoglycemia)
Prior or current infections (eg, skin, foot, dental, genitourinary)
Symptoms and treatment of chronic eye; kidney; nerve; genitourinary, bladder, and gastrointestinal function; heart; peripheral vascular; foot; and cerebrovascular complications
Nondiabetic medications that may affect blood glucose levels (eg, corticosteroids)
Risk factors for atherosclerosis, such as smoking, hypertension, obesity, dyslipidemia, and family history
History and treatment of other conditions, including endocrine and eating disorders
Family history of DM, endocrine disorders
Lifestyle, cultural, psychosocial, and economic factors that might influence DM management
Tobacco, alcohol, and/or controlled substance use
The physical examination includes assessment for orthostatic hypotension as a potential sign of autonomic neuropathy. A fundoscopic examination may give insight into the patient's risk of developing postoperative blindness, especially following prolonged spinal surgery in the prone position and cardiac surgery requiring cardiopulmonary bypass.
Type 1 DM is associated with a “stiff joint” syndrome, which poses a significant risk during airway management at the time of general anesthesia. Affecting the temporomandibular, atlantooccipital, and other cervical spine joints, these patients also tend to have short stature and waxy skin, related to chronic hyperglycemia and nonenzymatic glycosylation of collagen and its deposition in joints. A positive “prayer sign” can be elicited on examination with the patient unable to approximate the palmar surfaces of the phalangeal joints while pressing their hands together; this represents cervical spine immobility and the potential for a difficult endotracheal intubation.
Further airway evaluation should include assessment of thyroid gland size, as patients with type 1 DM have a 15% association of other autoimmune diseases, such as Hashimoto thyroiditis and Graves disease.
Finally, the degree of preoperative neurological dysfunction is important to document, especially prior to regional anesthesia or peripheral nerve blocks, to assess the degree of subsequent nerve injury.
The laboratory evaluation should include the following:
Hemoglobin A1C, serum glucose
Fasting lipid profile (total cholesterol, HDL cholesterol, triglycerides, LDL cholesterol)
Liver function tests (if abnormal, further evaluation for fatty liver or hepatitis)
Urinalysis (ketones, protein, sediment), microalbuminuria
Serum creatinine and estimated glomerular filtration rate
Serum electrolytes
Electrocardiogram
GENERAL PRE_OP MANAGEMENT
On the day of surgery, patients on oral regimens should be advised to discontinue these medications. Secretagogues (eg, sulfonylureas, meglitinides) have the potential to cause hypoglycemia. In addition, sulfonylureas have been associated with interfering with ischemic myocardial preconditioning and may theoretically increase risk of perioperative myocardial ischemia and infarction. Patients taking metformin should be advised to discontinue this drug because of the risk of developing lactic acidosis. For these patients, short-acting insulin may be administered subcutaneously as a sliding scale or as a continuous infusion, if needed, to maintain optimal glucose control, depending on the extent of surgery.
Patients who are insulin-dependent (type 1) should be advised to reduce their bedtime dose of insulin the night prior to surgery to prevent hypoglycemia, while nil by mouth. Maintenance insulin may be continued, based on history of glucose concentrations and the discretion of the advising clinician. Patients may be advised to consult their anesthesiologist and diabetes-managing practitioner for individualized recommendations regarding their situation. Additionally, patients should be monitored periodically preoperatively to assess for hyperglycemia and hypoglycemia.
DURING SURGERY
All patients undergoing surgery, under general anesthesia, require changing over to insulin from OHA and to regular insulin from intermediate acting insulin. Surgery should be scheduled in the morning. Omit BBF insulin. Do fasting blood sugar and put patient on GIK (Glucose-Insulin-Potassium) regimen according to blood sugar level at least one hour before starting surgery. The GIK regimen should continue at least one hour after the patient has taken the first postoperative meal and patient is shifted to pre-surgery thrice a day insulin regimen14.
During surgery do blood sugar at 1/2 hourly or one hourly interval as per the status of patient. Because of surgical stress, insulin requirements are more with intra-abdominal or thoracic surgery. CABG puts maximum surgical stress. The stress caused by laparotomy is much more than the stress caused by even whole body skin grafting.
Glucose-Insulin-Potassium (GIK) Regimen
Blood / Plasma Glucose mg.%
Fluid100 ml/hr.
InsulinU/100 ml
InsulinU/500 ml
KClmeq/100ml
< 100
10% Dextrose
1
5
2
100-200
10% Dextrose
2
10
2
200-300
10% Dextrose
3
15
2
300-400
10% Dextrose
4
20
2
>400
N / Saline
4
20
2
GOALS OF GLYCEMIC CONTROL
The goals for glycemic control are tailored to each patient based on a number of factors, such as nature of surgery, severity of underlying illness, modality used to achieve glycemic control, patient age, and sensitivity to insulin. Numerous clinical trials have involved various patient populations and examined the implications of perioperative hyperglycemia. Based on data derived from these studies, the American Diabetes Association has made recommendations for managing blood glucose levels in hospitalized patients with DM (see Table 1).
Table 1. American Diabetes Association Recommendations for Target Inpatient Blood Glucose Concentrations
Patient Population
Blood Glucose Target
Rationale
General medical/surgical
Fasting: 90-126 mg/dL Random: <180 mg/dL
Better outcomes, lower infection rates
Cardiac surgery
<150 mg/dL
Reduced mortality, reduced risk of sternal wound infections
Critically ill
80-110 mg/dL
Reduced mortality, morbidity (SICU); reduced morbidity; length of stay (MICU)
Acute neurological disorders
<110 mg/dL
Increased mortality if admission blood glucose >110 mg/dL
Prior to elective surgery, it is ideal for patients to have their HbA1c value at less than 6%. More stringent goals may further reduce complications; however, this is at the cost of increased risk of hypoglycemia. Less intensive glycemic control may be indicated in patients with severe or frequent episodes of hypoglycemia. Special populations, such as pregnant and elderly patients with DM, may require additional considerations. In addition, a plan for hypoglycemia should be delineated for individual patients.
Methods of Achieving Glycemic Control
Certain patients taking oral agents prior to surgery may be able to restart their previous regimen postoperatively; however, appropriateness of oral agents needs to be reassessed because of potential complications (see Table 2). Intravenous insulin is the most flexible and readily titratable agent, with few, if any, contraindications, making it an ideal agent for perioperative use.
Table 2. Considerations for Oral Agents
Class of Oral Agent
Example
Considerations
Secretagogues (eg, sulfonylureas, meglitinides)
Glyburide, glimepiride
Hypoglycemia, prolonged action, difficult to titrate
Biguanides
Metformin
Risk of lactic acidosis, use cautiously in renal or hepatic insufficiency, CHF
Thiazolidinediones
Rosiglitazone
Increased intravascular volume (CHF), slow onset of effect, difficult to titrate
The length, type of surgery, and degree of glycemic dysregulation will dictate the degree of supplemental intravenous insulin therapy. Patients with type 1 diabetes should have elective surgeries scheduled as the first case of the day to minimally disrupt their DM regimen. Depending on the length and extent of surgery, patients are often advised to administer half of their daily dose of long-acting insulin and to arrive at the preoperative admitting area early enough to have an intravenous infusion of dextrose instituted and their serum glucose monitored until the time of surgery. Perioperative methods for achieving tight glycemic control (80-110 mg/dL) are as follows:
Establish separate intravenous access for a “piggyback” infusion of regular insulin (50-100 U per 50-100 mL 0.9 saline, respectively). The infusion rate can be determined by using the formula: insulin (U/h) = serum glucose (mg/dL)/150. Intravenous glucose solution should be administered concomitantly to avoid hypoglycemia. Typically, a 5% dextrose solution is started when serum glucose levels are less than 150 mg/dL. Intra-arterial catheter placement is recommended to be able to sample glucose concentrations every 1-2 hours intraoperatively and postoperatively until a regimen of subcutaneous insulin or oral hypoglycemic agent is reinstituted. A second intravenous catheter is used for intravascular volume replacement with an isotonic saline solution.
. Use a computer-based system and set controls for intravenous insulin to achieve desired blood glucose level.
An example of such a system is the Glucommander®, presented at the 2003 Diabetes Technology meeting in San Francisco, CA; it is a novel method of attaining optimal glucose control by programming an intravenous infusion of insulin to respond to the measured serum glucose concentration. Initial parameters and baseline glucose value are entered. The program then recommends an insulin infusion rate and intervals to check subsequent glucose levels; this process may be repeated indefinitely. The amount of insulin recommended is based on a simple equation: insulin per hour = multiplier x (blood glucose – 60). Blood glucose concentrations are monitored as frequently as every 20 minutes up to a maximum interval specified in the initial orders. Typically, the monitoring interval is every hour, increasing when glucoses stabilize in the target range and decreasing if sugars are low or falling rapidly. The Glucommander® has been the successfully implemented in the critically ill as well as noncritically ill patient populations. However, intraoperative use has yet to be recommended..
PRE_OP ASSESSMENT
A comprehensive history and physical examination is imporatnt. Since estimates suggest that one third of diabetic patients are unaware of their disease, it may be prudent to screen all patients undergoing intermediate or major surgery by checking glycosylated hemoglobin (HbA1c).
The history should include the following:
Suggestive symptoms (eg, polyuria/polydipsia, blurred vision)
Eating patterns, nutritional status, exercise history, and weight history
Current treatment of diabetes, including medication regimen, diet, and glucose monitoring results
Frequency, severity, and etiology of acute complications (ie, ketoacidosis, hypoglycemia)
Prior or current infections (eg, skin, foot, dental, genitourinary)
Symptoms and treatment of chronic eye; kidney; nerve; genitourinary, bladder, and gastrointestinal function; heart; peripheral vascular; foot; and cerebrovascular complications
Nondiabetic medications that may affect blood glucose levels (eg, corticosteroids)
Risk factors for atherosclerosis, such as smoking, hypertension, obesity, dyslipidemia, and family history
History and treatment of other conditions, including endocrine and eating disorders
Family history of DM, endocrine disorders
Lifestyle, cultural, psychosocial, and economic factors that might influence DM management
Tobacco, alcohol, and/or controlled substance use
The physical examination includes assessment for orthostatic hypotension as a potential sign of autonomic neuropathy. A fundoscopic examination may give insight into the patient's risk of developing postoperative blindness, especially following prolonged spinal surgery in the prone position and cardiac surgery requiring cardiopulmonary bypass.
Type 1 DM is associated with a “stiff joint” syndrome, which poses a significant risk during airway management at the time of general anesthesia. Affecting the temporomandibular, atlantooccipital, and other cervical spine joints, these patients also tend to have short stature and waxy skin, related to chronic hyperglycemia and nonenzymatic glycosylation of collagen and its deposition in joints. A positive “prayer sign” can be elicited on examination with the patient unable to approximate the palmar surfaces of the phalangeal joints while pressing their hands together; this represents cervical spine immobility and the potential for a difficult endotracheal intubation.
Further airway evaluation should include assessment of thyroid gland size, as patients with type 1 DM have a 15% association of other autoimmune diseases, such as Hashimoto thyroiditis and Graves disease.
Finally, the degree of preoperative neurological dysfunction is important to document, especially prior to regional anesthesia or peripheral nerve blocks, to assess the degree of subsequent nerve injury.
The laboratory evaluation should include the following:
Hemoglobin A1C, serum glucose
Fasting lipid profile (total cholesterol, HDL cholesterol, triglycerides, LDL cholesterol)
Liver function tests (if abnormal, further evaluation for fatty liver or hepatitis)
Urinalysis (ketones, protein, sediment), microalbuminuria
Serum creatinine and estimated glomerular filtration rate
Serum electrolytes
Electrocardiogram
GENERAL PRE_OP MANAGEMENT
On the day of surgery, patients on oral regimens should be advised to discontinue these medications. Secretagogues (eg, sulfonylureas, meglitinides) have the potential to cause hypoglycemia. In addition, sulfonylureas have been associated with interfering with ischemic myocardial preconditioning and may theoretically increase risk of perioperative myocardial ischemia and infarction. Patients taking metformin should be advised to discontinue this drug because of the risk of developing lactic acidosis. For these patients, short-acting insulin may be administered subcutaneously as a sliding scale or as a continuous infusion, if needed, to maintain optimal glucose control, depending on the extent of surgery.
Patients who are insulin-dependent (type 1) should be advised to reduce their bedtime dose of insulin the night prior to surgery to prevent hypoglycemia, while nil by mouth. Maintenance insulin may be continued, based on history of glucose concentrations and the discretion of the advising clinician. Patients may be advised to consult their anesthesiologist and diabetes-managing practitioner for individualized recommendations regarding their situation. Additionally, patients should be monitored periodically preoperatively to assess for hyperglycemia and hypoglycemia.
DURING SURGERY
All patients undergoing surgery, under general anesthesia, require changing over to insulin from OHA and to regular insulin from intermediate acting insulin. Surgery should be scheduled in the morning. Omit BBF insulin. Do fasting blood sugar and put patient on GIK (Glucose-Insulin-Potassium) regimen according to blood sugar level at least one hour before starting surgery. The GIK regimen should continue at least one hour after the patient has taken the first postoperative meal and patient is shifted to pre-surgery thrice a day insulin regimen14.
During surgery do blood sugar at 1/2 hourly or one hourly interval as per the status of patient. Because of surgical stress, insulin requirements are more with intra-abdominal or thoracic surgery. CABG puts maximum surgical stress. The stress caused by laparotomy is much more than the stress caused by even whole body skin grafting.
Glucose-Insulin-Potassium (GIK) Regimen
Blood / Plasma Glucose mg.%
Fluid100 ml/hr.
InsulinU/100 ml
InsulinU/500 ml
KClmeq/100ml
< 100
10% Dextrose
1
5
2
100-200
10% Dextrose
2
10
2
200-300
10% Dextrose
3
15
2
300-400
10% Dextrose
4
20
2
>400
N / Saline
4
20
2
GOALS OF GLYCEMIC CONTROL
The goals for glycemic control are tailored to each patient based on a number of factors, such as nature of surgery, severity of underlying illness, modality used to achieve glycemic control, patient age, and sensitivity to insulin. Numerous clinical trials have involved various patient populations and examined the implications of perioperative hyperglycemia. Based on data derived from these studies, the American Diabetes Association has made recommendations for managing blood glucose levels in hospitalized patients with DM (see Table 1).
Table 1. American Diabetes Association Recommendations for Target Inpatient Blood Glucose Concentrations
Patient Population
Blood Glucose Target
Rationale
General medical/surgical
Fasting: 90-126 mg/dL Random: <180 mg/dL
Better outcomes, lower infection rates
Cardiac surgery
<150 mg/dL
Reduced mortality, reduced risk of sternal wound infections
Critically ill
80-110 mg/dL
Reduced mortality, morbidity (SICU); reduced morbidity; length of stay (MICU)
Acute neurological disorders
<110 mg/dL
Increased mortality if admission blood glucose >110 mg/dL
Prior to elective surgery, it is ideal for patients to have their HbA1c value at less than 6%. More stringent goals may further reduce complications; however, this is at the cost of increased risk of hypoglycemia. Less intensive glycemic control may be indicated in patients with severe or frequent episodes of hypoglycemia. Special populations, such as pregnant and elderly patients with DM, may require additional considerations. In addition, a plan for hypoglycemia should be delineated for individual patients.
Methods of Achieving Glycemic Control
Certain patients taking oral agents prior to surgery may be able to restart their previous regimen postoperatively; however, appropriateness of oral agents needs to be reassessed because of potential complications (see Table 2). Intravenous insulin is the most flexible and readily titratable agent, with few, if any, contraindications, making it an ideal agent for perioperative use.
Table 2. Considerations for Oral Agents
Class of Oral Agent
Example
Considerations
Secretagogues (eg, sulfonylureas, meglitinides)
Glyburide, glimepiride
Hypoglycemia, prolonged action, difficult to titrate
Biguanides
Metformin
Risk of lactic acidosis, use cautiously in renal or hepatic insufficiency, CHF
Thiazolidinediones
Rosiglitazone
Increased intravascular volume (CHF), slow onset of effect, difficult to titrate
The length, type of surgery, and degree of glycemic dysregulation will dictate the degree of supplemental intravenous insulin therapy. Patients with type 1 diabetes should have elective surgeries scheduled as the first case of the day to minimally disrupt their DM regimen. Depending on the length and extent of surgery, patients are often advised to administer half of their daily dose of long-acting insulin and to arrive at the preoperative admitting area early enough to have an intravenous infusion of dextrose instituted and their serum glucose monitored until the time of surgery. Perioperative methods for achieving tight glycemic control (80-110 mg/dL) are as follows:
Establish separate intravenous access for a “piggyback” infusion of regular insulin (50-100 U per 50-100 mL 0.9 saline, respectively). The infusion rate can be determined by using the formula: insulin (U/h) = serum glucose (mg/dL)/150. Intravenous glucose solution should be administered concomitantly to avoid hypoglycemia. Typically, a 5% dextrose solution is started when serum glucose levels are less than 150 mg/dL. Intra-arterial catheter placement is recommended to be able to sample glucose concentrations every 1-2 hours intraoperatively and postoperatively until a regimen of subcutaneous insulin or oral hypoglycemic agent is reinstituted. A second intravenous catheter is used for intravascular volume replacement with an isotonic saline solution.
. Use a computer-based system and set controls for intravenous insulin to achieve desired blood glucose level.
An example of such a system is the Glucommander®, presented at the 2003 Diabetes Technology meeting in San Francisco, CA; it is a novel method of attaining optimal glucose control by programming an intravenous infusion of insulin to respond to the measured serum glucose concentration. Initial parameters and baseline glucose value are entered. The program then recommends an insulin infusion rate and intervals to check subsequent glucose levels; this process may be repeated indefinitely. The amount of insulin recommended is based on a simple equation: insulin per hour = multiplier x (blood glucose – 60). Blood glucose concentrations are monitored as frequently as every 20 minutes up to a maximum interval specified in the initial orders. Typically, the monitoring interval is every hour, increasing when glucoses stabilize in the target range and decreasing if sugars are low or falling rapidly. The Glucommander® has been the successfully implemented in the critically ill as well as noncritically ill patient populations. However, intraoperative use has yet to be recommended..
Insulin Type
Synonyms
Retardant
Time of Effect Hours Onset Peak Duration
Unmodified
SolubleRegular
None
0.25-1H] P] sameB
1.5-4
5-9
NPH
Isophane
Protamine
0-5-2H]P] sameB]
3-6
8-14
Lente
Mixture of 30% Semilente (an amorphous precipitate of Insulin with Zinc ions) with 70% Ultralente Insulin
Zinc
H 1-2P 1-2B 1-5-3
3-83-85-10
7-147-1610-24
Ultralente
An Insoluble Crystal of Zinc and Insulin
Zinc
H 2-3B 3-4
4-86-12
8-1412-28
Insulin Analogues
Lispro
None
5-15 Minutes
1-2
4-5
Premixed
10/9025/7530/70 and 50/50
Protamine
0.25-1.5
3-6
8-14
Insulin regimens
Once daily regimenIt is most commonly used in type 2 diabetes patients with secondary failure to OHA and used in combination with OHA. Either lente, ultralente, or NPH is used. NPH is preferred before breakfast, whereas lente or ultralente before dinner. The regimen is not suitable for type 1 diabetes cases.
Twice daily regimen It is the most commonly used regimen as it is suitable for most type l, 2, and GDM patients. It is very convenient as patient has to take only BBF and before dinner (BD) dose and there is no need to carry insulin to school or office. Usually both short and long acting insulins are used in combination, but in few cases only long acting insulin can be used alone but not the short acting. This regimen is not to be used in acute medical emergencies. Usually, of the total daily dose 2/3rd is given BBF and 1/3rd before dinner; but depending upon eating habits and glycaemic status, dose can vary and even 50 percent can be given BBF and BD. Again, the usual ratio of long acting to short acting is 2/3:1/3 or 70:30. But in premixed insulins wide range is available from 10:90, 25:75 to 50:50. This regimen gives similar results as compared to multiple injections or CSII by pump.
Basal bolus regimenIn this regimen regular and intermediate acting insulin is used. Basal requirement is met by intermediate acting insulin given twice a day before breakfast and dinner. The regular insulin is given before each meal thrice a day. Out of the total daily requirement 50 percent is given as basal (intermediate) and 50% as regular insulin. The share of regular insulin (50%) is given as 20% BBF, 10% BL and 20% BD. It gives similar results as compared to twice a day but the only disadvantage is that the before lunch (BL) dose is to be taken at school or office.
Continuous subcutaneous insulin infusion Only short acting insulin is used and is given by insulin pump that the patient has to wear throughout the day. It is neither practical, nor are the results better than twice daily or bolus regimen.
Insulin therapy for ketoacidosis
The use of low dose insulin regimen either given by insulin infusion or intramuscularly is now the accepted regimen for keto-acidosis. The high dose regimen is no longer used, as with low dose regimen there is less frequent hypokalemia, hypoglycemia, and more predictable response.
Insulin is given as 6 u/hour by continuous IV infusion. Only short acting insulin is used. When the blood sugar falls to 250 mg% the normal saline is replaced with 10% dextrose and insulin infusion rate reduced to 4 u/hour. But if significant drop in plasma glucose is not observed after 2 hours of insulin infusion and if fluid replacement, blood pressure, and infusion lines are satisfactory, then double the infusion rate.
Insulin can be given by IM route with dose of 6 u/hr but often a loading does of 20 u is required. If after 2 hours the fall in sugar is not satisfactory, either double the dose or start IV infusion. The acidosis and ketosis resolve more slowly than hyperglycemia; hence, IV dextrose preferably 10% dextrose with insulin should continue till patient starts eating and shift to thrice a day regimen by subcutaneous route. It is advisable to increase the total daily dose by 20 prcent of previous (before onset of ketoacidosis) insulin dose and after recovery discharge on previous or twice a day regimen.
Insulin regimen in special group of patients
Elderly: Do not aim for strict glycemic control. Twice a day or once a day regimen are most suitable.
Renal failure: There is considerable reduction in insulin requirement and twice daily or basal bolus regimens are suitable.
Recurrent hypoglycemia: Insulin dose distribution needs to be reviewed rather than the regimen. In some cases shifting evening dose to bedtime can prevent nocturnal hypoglycemia.
Children: Same regimens are used as for adults. Intermediate insulin may be absorbed faster. Twice a day is best suited as it eliminates injection at school.
Secondary diabetes: Due to pancreatic disease; usually have mild diabetes and can be managed with twice a day regimen.
Steroid and endocrine diabetes: They have marked insulin insensitivity and considerable endogenous insulin secretions. It may require high dose of insulin, but cessation of steroids often allows patient to come off insulin again. They are managed with twice daily regimen. Endocrinopathies cause mild diabetes that can be easily controlled with twice a day insulin regimen.
Pregnancy: Insulin dose will increase as pregnancy advances and balance of insulin changing to greater daytime requirement. There is sudden fall in insulin requirement after delivery.
Cirrhosis of liver: Marked insulin insensitivity during day but because of impaired gluconeogenesis, no difficulty in maintaining glucose concentration over night. Hence require preprandial injection regimen.
Synonyms
Retardant
Time of Effect Hours Onset Peak Duration
Unmodified
SolubleRegular
None
0.25-1H] P] sameB
1.5-4
5-9
NPH
Isophane
Protamine
0-5-2H]P] sameB]
3-6
8-14
Lente
Mixture of 30% Semilente (an amorphous precipitate of Insulin with Zinc ions) with 70% Ultralente Insulin
Zinc
H 1-2P 1-2B 1-5-3
3-83-85-10
7-147-1610-24
Ultralente
An Insoluble Crystal of Zinc and Insulin
Zinc
H 2-3B 3-4
4-86-12
8-1412-28
Insulin Analogues
Lispro
None
5-15 Minutes
1-2
4-5
Premixed
10/9025/7530/70 and 50/50
Protamine
0.25-1.5
3-6
8-14
Insulin regimens
Once daily regimenIt is most commonly used in type 2 diabetes patients with secondary failure to OHA and used in combination with OHA. Either lente, ultralente, or NPH is used. NPH is preferred before breakfast, whereas lente or ultralente before dinner. The regimen is not suitable for type 1 diabetes cases.
Twice daily regimen It is the most commonly used regimen as it is suitable for most type l, 2, and GDM patients. It is very convenient as patient has to take only BBF and before dinner (BD) dose and there is no need to carry insulin to school or office. Usually both short and long acting insulins are used in combination, but in few cases only long acting insulin can be used alone but not the short acting. This regimen is not to be used in acute medical emergencies. Usually, of the total daily dose 2/3rd is given BBF and 1/3rd before dinner; but depending upon eating habits and glycaemic status, dose can vary and even 50 percent can be given BBF and BD. Again, the usual ratio of long acting to short acting is 2/3:1/3 or 70:30. But in premixed insulins wide range is available from 10:90, 25:75 to 50:50. This regimen gives similar results as compared to multiple injections or CSII by pump.
Basal bolus regimenIn this regimen regular and intermediate acting insulin is used. Basal requirement is met by intermediate acting insulin given twice a day before breakfast and dinner. The regular insulin is given before each meal thrice a day. Out of the total daily requirement 50 percent is given as basal (intermediate) and 50% as regular insulin. The share of regular insulin (50%) is given as 20% BBF, 10% BL and 20% BD. It gives similar results as compared to twice a day but the only disadvantage is that the before lunch (BL) dose is to be taken at school or office.
Continuous subcutaneous insulin infusion Only short acting insulin is used and is given by insulin pump that the patient has to wear throughout the day. It is neither practical, nor are the results better than twice daily or bolus regimen.
Insulin therapy for ketoacidosis
The use of low dose insulin regimen either given by insulin infusion or intramuscularly is now the accepted regimen for keto-acidosis. The high dose regimen is no longer used, as with low dose regimen there is less frequent hypokalemia, hypoglycemia, and more predictable response.
Insulin is given as 6 u/hour by continuous IV infusion. Only short acting insulin is used. When the blood sugar falls to 250 mg% the normal saline is replaced with 10% dextrose and insulin infusion rate reduced to 4 u/hour. But if significant drop in plasma glucose is not observed after 2 hours of insulin infusion and if fluid replacement, blood pressure, and infusion lines are satisfactory, then double the infusion rate.
Insulin can be given by IM route with dose of 6 u/hr but often a loading does of 20 u is required. If after 2 hours the fall in sugar is not satisfactory, either double the dose or start IV infusion. The acidosis and ketosis resolve more slowly than hyperglycemia; hence, IV dextrose preferably 10% dextrose with insulin should continue till patient starts eating and shift to thrice a day regimen by subcutaneous route. It is advisable to increase the total daily dose by 20 prcent of previous (before onset of ketoacidosis) insulin dose and after recovery discharge on previous or twice a day regimen.
Insulin regimen in special group of patients
Elderly: Do not aim for strict glycemic control. Twice a day or once a day regimen are most suitable.
Renal failure: There is considerable reduction in insulin requirement and twice daily or basal bolus regimens are suitable.
Recurrent hypoglycemia: Insulin dose distribution needs to be reviewed rather than the regimen. In some cases shifting evening dose to bedtime can prevent nocturnal hypoglycemia.
Children: Same regimens are used as for adults. Intermediate insulin may be absorbed faster. Twice a day is best suited as it eliminates injection at school.
Secondary diabetes: Due to pancreatic disease; usually have mild diabetes and can be managed with twice a day regimen.
Steroid and endocrine diabetes: They have marked insulin insensitivity and considerable endogenous insulin secretions. It may require high dose of insulin, but cessation of steroids often allows patient to come off insulin again. They are managed with twice daily regimen. Endocrinopathies cause mild diabetes that can be easily controlled with twice a day insulin regimen.
Pregnancy: Insulin dose will increase as pregnancy advances and balance of insulin changing to greater daytime requirement. There is sudden fall in insulin requirement after delivery.
Cirrhosis of liver: Marked insulin insensitivity during day but because of impaired gluconeogenesis, no difficulty in maintaining glucose concentration over night. Hence require preprandial injection regimen.
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