10. • Investigations-
1.urine phosphorus excretion(renal excretion >100mg
by 24 hour urine collection or a fractional excretion of
phosphate >5% during hypophosphatemia indicates
renal loss)
2.vitamin d estimation
3.intact PTH
11. • Treatment
1.Acute moderate(1.0-2.5 mg/dl)-
no specific treatment if asymptomatic, treat underlying
cause
2.Acute severe(<1.0 mg/dl)-
iv phosphate therapy(potassium phosphate, sodium
phosphate)
13. Hypermagnesemia
• Serum magnesium >2.2 mEq/L
• Causes-
1.Iatrogenic(large doses of magnesium containing
antacids or laxatives, during treatment of pre-eclampsia
with i.v magnesium, therapeutic doses of antacids in
renal insufficiency)
2.ESRD
16. • Clinical features
-Signs and symptoms when magnesium level >4mEq/l
1.Neuromuscular abnormalities-
-hyporeflexia(1st sign)
-lethargy and weakness
-progression to paralysis, diaphragmatic involvement,
leading to respiratory failure
20. Hypomagnesemia
• Serum magnesium less than 1.46 mg/dL)
• Hypomagnesemia can be attributed to chronic
disease, alcohol use disorder, gastrointestinal losses,
renal losses, and other conditions. Signs and
symptoms of hypomagnesemia include anything
from mild tremors and generalized weakness to
cardiac ischemia and death
21. • Causes
1.Hypomagnesemia can be secondary to
decreased intake, as seen in:
-Startvation
-Alcohol use disorder
-Critically ill patients who are receiving total
parenteral nutrition
22. 2.It also can be secondary to the following medications:
-Loop and thiazide diuretics
-Proton pump inhibitors
-Aminoglycoside antibiotics
-Amphotericin B
-Digitalis
-Chemotherapeutic drugs, such as cisplatin,
cyclosporine
23. 3.Hypomagnesemia can be induced by gastrointestinal
and/or renal losses,
-Acute diarrhea
-Chronic diarrhea
-Hungry bone syndrome
24. -Acute pancreatitis
-Gastric bypass surgery
-Inherited tubular disorders (Gitelman
syndrome, Bartter syndrome)
-Familial hypomagnesemia with hypercalciuria
and nephrocalcinosis
26. 2. Cardiovascular Manifestations
-Electrocardiogram changes, including widening of the
QRS complex, peaked T waves, prolongation of the PR
interval
-Atrial and ventricular premature systoles
-Atrial fibrillation
-Ventricular arrhythmias
-Cardiac ischemia
27. 3.Other Electrolyte and Hormone Abnormalities
-Hypocalcemia
-Hypoparathyroidism
-Hypokalemia
29. • Treatment
-If a patient is hemodynamically unstable in an acute
hospital setting, 1 to 2 grams of magnesium sulfate can
be given in about 15 minutes.
-For symptomatic, severe hypomagnesemia in a stable
patient, 1 to 2 grams of magnesium sulfate can be
given over one hour.
30. -Non-emergent repletion of the adult patient is
generally 4 to 8 grams of magnesium sulfate given
slowly over 12 to 24 hours. In pediatric patients, the
dose is 25 to 50 mg/kg (with a maximum of 2 grams).
-For an asymptomatic patient who is not hospitalized
and can tolerate medications by mouth, sustained-
release oral replacement should be tried first
31. HYPERTENSION
• Hypertension is defined as the presence of blood
pressure elevation to a level that places patients at
increased risk for target organ damage in several
vascular beds including the retina, brain, kidneys and
large conduit arteries.
• Stage 1 hypertension(SBP 130-139 or DBP 80-
89mmhg)
• Stage 2(SBP >140 or DBP>90)
32. • Hypertensive urgencies-DBP >120mmhg,warrant bp
reduction within several hours. Associated with
hypertension with optic disc edema, progressive
end-organ complications rather than damage.
• Hypertensive emergencies include accelerated
hypertension, SBP >180mmhg, DBP>120mmhg
presenting with headaches, blurred vision or focal
neurological symptoms and malignant
hypertension(requires presence of pappiloedema)
33. *Hypertensive emergencies requires immediate bp
reduction by 20-25% over first hour to prevent or
minimize end organ damage
• Resistant hypertension-B.p >130/80 mmhg in
hypertensive patient on >3 antihypertensives agents
one of which is diuretic or controlled b.p on >4
antihypertensives.
34. RENAL PHYSIOLOGY
• MAJOR FUNCTIONS OF THE KIDNEY
Regulation of body fluid volume
Regulation of osmotic balance
Regulation of electrolyte composition
Regulation of acid-base balance
Regulation of blood pressure
Erythropoiesis
Excretion of waste products and
Foreign substances
36. • QUANTITIES OF SOLUTE FILTERED AND EXCRETED
Plasma conc. Of solutes & Percent reabsorbed
Na 140 ,99+
Cl 105 ,99+
HCO3 25 99+
K 4 86+
Glucose 5 100%
Urea 5 60%
37. • The main role of the kidneys is to filter the circulating
blood in order to remove from the body waste
products acquired through direct ingestion or
resulting from catabolism of the organism. The
removal of these products is meant to avoid their
accumulation to toxic levels
38. • A second critical role of the kidneys is to regulate and
try to maintain within normal levels the extracellular
fluid, circulating blood volume and, as a
consequence, the blood pressure. This is achieved by
regulating the volume of electrolytes and fluid which
is excreted in urine and also through the production
and release of enzymes by the rennin angiotensin
system, leading to the production of vasoactive
compounds.
39. • The kidney also has an endocrine role which
contributes to several rather important physiological
activities. It contributes to the regulation of red
blood cell through production or erythropoietin.
40. • Regulates diuresis through increased renal blood
flow as a result of production of urodilatin and,
calcium absorption through conversion of 25-
hydroxycholecalciferol to 1,25-
dihydroxycholecalciferol, the active form of Vitamin
D3. The kidneys also secrete renin, an enzyme
involved in the production of angiotensin II, leading
to synthesis and release of aldosterone
41. • The final role attributed to the kidney is in
gluconeogenesis. Tubular cells of the kidney are
capable of using amino acids from circulation to
make glucose and export it to circulation as the liver
does. The main difference appears to be that liver
operates more in a circadian rhythm according to
food intake, while kidneys produce a continuous
supply of glucose
42. RENAL BLOOD SUPPLY
• The kidney is irrigated through the renal
artery which branches of the abdominal aorta.
The renal artery enters through the hilus of
the kidney into the renal sinus and divides into
several segmental arteries which in turn give
rise to the interlobar and arcuate arteries
43. • These travel through the renal column towards the
cortex of the kidney and upon reaching the base of
the pyramids they follow the base projecting
interlobular arteries towards the cortex and these, in
turn divide into the afferent arterioles that brings
blood to each glomerulus forming the glomerular
capillaries within each renal corpuscle.
44. • Exiting the renal corpuscle the glomerular capillaries
coalesce into the efferent arteriole which, intimately
associated with each nephron, form a plexus named
peritubular capillaries in close apposition with the
proximal and distal convoluted tubules of each
nephron. The peritubular capillaries then travel into
the medulla where it becomes the vasa recta which
are in close contact with the loop of Henle of the
juxtamedullary nephrons.
45. • Finally, the vasa recta join and become the
interlobular vein leaving the cortex into the arcuate
vein.
• Several arcuate veins form the interlobar vein which
travels through the renal column towards the renal
vein.
• This in turn leaves the kidney through the renal sinus
and joins general circulation through a connexion to
the inferior vena cava
46. URINE ANALYSIS
• Urine analysis involves assessment of urine
characteristics to aid in disease diagnosis and
consists of physical observation, chemical, and
microscopic analysis.
47. • Physical observation involves assessing color and
clarity. The normal color of urine is straw colored in
the presence of dehydration urine is a darker color.
Red urine may indicate hematuria or porphyria or
represent the dietary intake of food like beets.
Cloudy urine may be seen in the presence of pyuria
due to urinary tract infection.
48. • Specific gravity is an indicator of renal concentrating
ability may be measured using refractometry or
chemically by use of urine dipstick. The physiologic
range for specific gravity is 1.003 to 1.030 and is
increased with concentrated urine and decreased
with dilute urine.
49. • Urine dipstick provides qualitative analysis of
different analytes in urine using chemical analysis.
• Dipstick uses dry chemistry methods to detect for
the presence of protein, glucose, blood, ketones,
bilirubin, urobilinogen, nitrite, and leukocyte
esterase. These may be performed as a point-of-care
test near a patient. The color changes following
interaction of the urine with the chemical reagents
impregnated on the paper of the dipstick are
compared to the color chart guide to interpret the
results.
50. • In normal urine RBC per high-power field is between
0 to 3 and white blood cells (WBC) between 0 to 5.
Ketones are present in fasting, severe vomiting, or
diabetic ketoacidosis. Urine dipstick only detects
acetoacetate and acetone, not the ketone beta-
hydroxybutyrate..
51. • Bilirubin is detected in the presence of conjugated
hyperbilirubinemia, urobilinogen may normally be
present but is absent in conjugated
hyperbilirubinemia and increased in the presence of
prehepatic jaundice and hemolysis. Nitrite and
leucocyte esterase are indicators of urinary tract
infection. Some bacteria, for example,
Enterobacteriaceae, convert nitrates to nitrites
52. • The microscopic analysis involves wet-prep analysis
of urine to assess in the presence of cells, casts, and
crystals as well as micro-organisms. Red blood casts
usually denote glomerulonephritis while white blood
cell casts are consistent with pyelonephritis.
Presence of white blood cells and WBC casts
indicates infection; red blood cells indicate renal
injury; RBC casts indicate tubular damage or
glomerulonephritis. Hyaline casts consist of protein
and may occur in glomerular disease.
53. • Crystals may also be identified in urine and are
indicative of the following conditions:
-Triple phosphate in pseudogout.
-Uric acid crystals associated with gout.
-Oxalate crystals in ethylene glycol poisoning or primary
and secondary hyperoxaluria.
-Cystine in cystinuria.
54. • The best specimen for urine analysis is a freshly
voided midstream urine. Midstream urine is utilized
as it is less likely to be contaminated by commensal
bacteria and epithelial cells.
55. • Albuminuria and Proteinuria
• Albuminuria is used as a marker for detection of
incipient nephropathy in diabetics; it is an
independent marker for the cardiovascular
disease since it connected increased endothelial
permeability and is also a marker of chronic renal
impairment. Urine albumin may be measured in
24-hour urine collections or early
morning/random specimens as an
albumin/creatinine ratio.
56. • Presence of albuminuria on two occasions with the
exclusion of a urinary infection indicates glomerular
dysfunction. The presence of albuminuria for 3 or
more months is indicative of chronic kidney disease.
57. • Frank proteinuria is defined as greater than 300 mg
per day of protein. Normal urine protein up to 150
mg per day (30% albumin; 30% globulins; 40% Tamm
Horsfall protein). Increased amounts of protein in
urine may be due to:
-Glomerular proteinuria: Caused by defects in perm
selectivity of the glomerular filtration barrier to plasma
proteins (for example, glomerulonephritis or nephrotic
syndrome)
-Tubular proteinuria: Caused by incomplete tubular
reabsorption of proteins (for example, interstitial
nephritis)
58. • Overflow proteinuria: Caused by increased plasma
concentration of proteins (for example, multiple
myeloma-Bence Jones protein,
myoglobinuria),Urinary tract inflammation or tumor
• Urine protein may be measured using either a 24-
hour urine collection or random urine protein:
creatinine ratio (early morning sample preferred and
more representative of the 24-hour sample).
59. RENAL BIOCHEMISTRY
• There are a number of clinical laboratory tests
that are useful in investigating and evaluating
kidney function. Clinically, the most practical
tests to assess renal function is to get an
estimate of the glomerular filtration rate (GFR)
and to check for proteinuria (albuminuria).
60. • Glomerular Filtration Rate
-The best overall indicator of the glomerular function is
the glomerular filtration rate (GFR). The normal GFR for
an adult male is 90 to 120 mL per minute. GFR is the
rate in milliliters per minutes at which substances in
plasma are filtered through the glomerulus, in other
words, the clearance of a substance from the blood.
61. The characteristics of an ideal marker of GFR are as
follows:
-It should appear endogenously in the plasma at a
constant rate
-It should be freely filtered at the glomerulus
-It can be neither reabsorbed nor secreted by the renal
tubule
-It should not undergo extrarenal elimination.
62. • Creatinine
-The most commonly used endogenous marker for
assessment of glomerular function is creatinine. The
calculated clearance of creatinine is used to provide an
indicator of GFR. This involves the collection of urine
over a 24-hour period or preferably over an accurately
timed period of 5 to 8 hours since 24-hour collections
are notoriously unreliable.
63. • Creatinine clearance is then calculated using the
equation:
C = (U x V) / P
C = clearance, U = urinary concentration, V = urinary
flow rate (volume/time ie ml/min), and P = plasma
concentration
64. • Creatinine is the by-product of creatine phosphate in
muscle, and it is produced at a constant rate by the
body. For the most part, creatinine is cleared from
the blood entirely by the kidney. Decreased
clearance by kidney results in an increased blood
creatinine. The amount of creatinine produced per
day depends on muscle bulk, and thus, there is a
difference in creatinine ranges between males and
females with lower creatinine values in children and
those with decreased muscle bulk..
65. • Diet also influences creatinine values. Creatinine can
change as much as 30% after ingestion of red meat.
As GFR increases in pregnancy lower creatinine
values are found in pregnancy. Additionally, serum
creatinine is a later indicator of renal impairment-
renal function is decreased by 50% before a rise in
serum creatinine is observed
66. • Serum creatinine is also utilized in GFR estimating
equations such as the Modified Diet in Renal Disease
(MDRD) and the CKD-EPI equation. These eGFR
equations are superior to serum creatinine alone
since they include race, age, and gender variables.
GFR is classified into the following stages based on
the kidney disease.
67. • Improving Global Outcomes (KDIGO) stages of
chronic kidney disease (CKD):
-Stage 1 GFR greater than 90 ml/min/1.73 m
-Stage 2 GFR-between 60 to 89 ml/min/1.73 m
-Stage 3a GFR 45 to 59 ml/min/1.73 m
-Stage 3b GFR 30 to 44 ml/min/1.73 m
-Stage 4 GFR of 15 to 29 ml/min/1.73 m
-Stage 5-GFR less than 15 ml/min/1.73 m (ESRD)
68. • Blood Urea Nitrogen (BUN)
-BUN is a nitrogen-containing compound formed in the
liver as the end product or protein metabolism and
urea cycle. About 85% of urea is eliminated via kidneys;
the rest is excreted via the gastrointestinal (GI) tract.
Serum urea is increased in acute and chronic renal
failure/impairment). Urea may also increase in other
conditions not related to renal diseases such as upper
GI bleeding, dehydration, catabolic states, and high
protein diets. Urea may be decreased in starvation,
low-protein diet, and severe liver disease.
-
69. • The ratio of BUN:Creatinine can be useful to
differentiate prerenal from renal causes when the
BUN is increased. In pre-renal disease the ratio is
close to 20:1, while in intrinsic renal disease it is
closer to 10:1.
• Cystatin C
-Cystatin C is a low-molecular-weight protein which
functions as a protease inhibitor produced by all
nucleated cells in the body. Serum levels of cystatin C
are inversely correlated with the glomerular filtration
rate (GFR). Cystatin C is measured in serum and urine.
The advantages of cystatin C over creatinine are that it
is not affected by age, muscle bulk, or diet.
70. • Tests of Tubular Function
-The renal tubules play an important role in
reabsorption of electrolytes, water, and maintaining
acid-base balance. Electrolytes, sodium, potassium,
chloride, magnesium, phosphate can be measured in
urine as well as glucose. Measurement of urine
osmolality allows for assessment of concentrating
ability of urine tubules. A urinary osmolality greater
than 750 mOsmol/Kg H2O implies a normal
concentrating ability of tubules.
71. RENAL RADIOIMAGING
• PLAIN X-RAY
-Radiographic features
length should not be less than three vertebral body
lengths, and no more than four vertebral body
lengths 10.
• CT
-on unenhanced CT, the renal pyramids can appear
hyperdense
72. • Ultrasound
-Antenatally, fetal kidneys show varying texture
depending on gestational age. It is echogenic in the first
trimester, with decreasing echogenicity as the
pregnancy progresses. Corticomedullary differentiation
can be appreciated after 15 weeks of gestation but
clear demarcation between cortex and medulla can be
seen at 20 weeks. Renal echogenicity decreases
compared to liver
73. -Normal kidney appearance in adult :
• cortex is less echogenic than the liver
• medullary pyramids are slightly less echogenic than the cortex
• cortex thickness equals/is more than 6 mm
• if the pyramids are difficult to differentiate, the parenchymal
thickness can be measured instead and should be 15-20 mm
• central renal sinus, consisting of the calyces, renal pelvis and fat, is
more echogenic than the cortex
• renal pelvis may appear as a central slit of anechoic fluid at the
hilum
• normal ureters are generally not well seen on ultrasound
74. APPLIED ANATOMY OF NECK
• The neck is limited superiorly by the inferior border
of the mandible, anteriorly by midline, inferiorly by
the superior border of the clavicle, and posteriorly by
the anterior margin of the trapezius muscle. Many of
the reported anatomical triangles of the neck have
been depicted and mainly classified within the
broader anterior and posterior cervical triangles .
75. • The neck also contains such triangles as the
suboccipital triangle in the posterior aspect of the
neck, the triangle of the vertebral artery and scalene
triangle in deep layer of the neck, Lesser's, Pirogov's,
Béclard's, and Farabeuf's triangles . These anatomical
triangles contain nerves, vessels, and other
anatomical structures.
76.
77. • Anterior Triangle of the Neck
-The anterior cervical triangle is bounded by the
midline of the neck, the anterior border of the
sternocleidomastoid muscle (SCM), and the inferior
border of the mandible [3]. This triangle is typically
subdivided into three paired and one unpaired triangle.
The three paired triangles are the submandibular
(digastric), carotid, and muscular triangles. The
unpaired triangle is the submental triangle.
78. • Submandibular (digastric) triangle
-The anterior and posterior borders of the submandibular
triangle are the anterior and posterior bellies of the
digastric muscle, respectively, and the base is the inferior
border of the mandible. The floor of this triangle is formed
by the mylohyoid muscle. The attachment of the mylohyoid
muscle onto the mandible is more inferiorly in the anterior
region and more superiorly in the posterior region of the
triangle. For this reason, odontogenic inflammation caused
by lower molar tooth infection, especially the wisdom
teeth, could easily spread below the mylohyoid muscle into
the submandibular space.
79. • This triangle usually contains the marginal
mandibular branch of the facial nerve (MMB), the
facial and lingual arteries and veins, the
submandibular gland and lymph nodes, the nerve to
the mylohyoid, the hypoglossal nerve, and the lower
pole of the parotid gland. The submandibular
incision to access to this triangle, e.g., abscess
drainage and submandibulectomy, should be inferior
to the MMB.
80.
81. • Lesser's triangle
-It is bounded by the anterior and posterior bellies of
the digastric muscle and the hypoglossal nerve.The
most important structure in it is the lingual artery. The
floor of Lesser's triangle is the hyoglossus muscle, and
the lingual artery is found beneath it.It is an ideal
location for accessing the lingual artery, especially to
control severe hemorrhage in the oral floor when it is
injured . The lingual foramen is where the sublingual or
submental artery enters the mandible.
82. • Carotid triangle
-The carotid triangle is bordered by the posterior belly
of the digastric muscle, the superior belly of the
omohyoid muscle, and the anterior border of the SCM.
The floor and medial wall of this triangle is formed by
the hyoglossus, thyrohyoid, and inferior and middle
pharyngeal constrictor muscles. In the normal position,
the inferior border of this triangle reaches the level of
the carotid tubercle (anterior tubercle of the transverse
process of the C6).
83. -The carotid triangle includes the common carotid
artery and its bifurcation into the external carotid
artery (ECA) and internal carotid artery (ICA). It usually
contains the superior thyroid, lingual, facial, occipital,
and ascending pharyngeal arteries. The superior
thyroid, lingual, facial, ascending pharyngeal, and
occipital veins accompany with these arteries, and all of
them drain into the internal jugular vein (IJV). The
hypoglossal nerve travels across the ECA and ICA. The
external and internal branches of the superior laryngeal
nerve arising from the vagus nerve can be identified
medial to the ECA below the hyoid bone.
84. • Farabeuf's triangle
-Within the carotid triangle. The boundaries of this
triangle are the IJV, the common facial vein, and the
hypoglossal nerve and direct its base superiorly. This
triangle was constantly located within the carotid
triangle and included at least one of the branches of
the common carotid artery. The carotid bifurcation was
contained within this triangle on two sides.This triangle
is a helpful landmark in extensive dissections of the
neck, especially in locating the IJV, the safety of which
is best conserved by promptly exposing it.
85. • Posterior Triangle of the Neck
-The posterior cervical triangle is bounded by the
posterior border of the SCM anteriorly, the anterior
border of the trapezius muscle posteriorly, and middle
one-third of the clavicle inferiorly. Its floor is covered
with the prevertebral layer of the deep cervical fascia.
86. • The posterior cervical triangle is subdivided into
occipital and supraclavicular (subclavian or
omoclavicular) triangles by the omohyoid muscle. It
contains the accessory lymph nodes, the inferior deep
lymph nodes, the transverse cervical lymph nodes, the
suprascapular artery, the subclavian artery, the
external jugular vein (EJV), the accessory nerve, great
auricular nerve, transverse cervical nerve,
supraclavicular nerve, the inferior belly of the
omohyoid, and branches of the thyrocervical trunk. It
also includes branches to the levator scapulae, serratus
anterior and rhomboid muscles.
87. • Supraclavicular triangle
-The supraclavicular triangle is a clinically important
anatomical area. Diseases of the vessels and lymph nodes
located in it cause various clinical syndromes. This triangle is
the anterior division of the posterior cervical triangle. The
anterior and inferior borders are the same as those of the
posterior cervical triangle, but the superior border is the
inferior belly of the omohyoid. It corresponds to the
supraclavicular fossa, which is immediately above the
clavicle.It is bounded by the superficial and deep fasciae and
the platysma muscle, and the supraclavicular nerves travel
across it.
88. • It mainly contains the subclavian artery and vein, and
the brachial plexus. The trunks of the brachial plexus
and the subclavian artery can be palpated with an
examining finger. The suprascapular vessels and
dorsal scapular artery run transversely across the
triangle. The EJV runs behind the posterior border of
the SCM to end in the subclavian vein.
89. APPLIED ANATOMY OF FEMORAL
TRIANGLE
• The femoral triangle is a hollow area in the anterior
thigh. Many large neurovascular structures pass
through this area, and can be accessed relatively
easily. Thus, it is an area of both anatomical and
clinical importance.
90. • Borders
-Superior border – Formed by the inguinal ligament, a
ligament that runs from the anterior superior iliac spine
to the pubic tubercle.
-Lateral border – Formed by the medial border of the
sartorius muscle.
-Medial border – Formed by the medial border of the
adductor longus muscle. The rest of this muscle forms
part of the floor of the triangle.
91. • Floor and a roof:
-Anteriorly, the roof of the femoral triangle is formed
by the fascia lata.
-Posteriorly, the base of the femoral triangle is formed
by the pectineus, iliopsoas and adductor longus
muscles.
-The inguinal ligament acts as a flexor retinaculum,
supporting the contents of the femoral triangle during
flexion at the hip.
92.
93. • Contents (lateral to medial):
-Femoral nerve – Innervates the anterior compartment
of the thigh, and provides sensory branches for the leg
and foot.
-Femoral artery – Responsible for the majority of the
arterial supply to the lower limb.
-Femoral vein – The great saphenous vein drains into
the femoral vein within the triangle.
-Femoral canal – A structure which contains deep
lymph nodes and vessels.
94. • Clinical Relevance: The Femoral Triangle
1.Access to the Femoral Artery
-The femoral artery is located superficially within the
femoral triangle, and is thus easy to access. This makes
it suitable for a range of clinical procedures such as
coronary angiography
2.Access to the femoral vein
-The femoral vein is located medial to femoral artery,
and is used for femoral catheterisation for dialysis.
97. • The arterial supply to the upper limb is delivered via
five main vessels (proximal to distal):
-Subclavian artery
-Axillary artery
-Brachial artery
-Radial artery
-Ulnar artery
98.
99. • Clinical Relevance: Axillary Artery Aneurysm
-An axillary artery aneurysm is a dilation of the vessel to more
than twice its original size. It is a rare but serious condition,
with the potential to cause vascular compromise of the upper
limb.
-The dilated portion of the axillary artery can compress the
brachial plexus, producing neurological symptoms such as
paraesthesia and muscle weakness.
-The definitive treatment of an axillary artery aneurysm is
surgical. It involves excising the aneurysm and reconstructing
the vessel wall using a vascular graft.
100. • Clinical Relevance: Occlusion or Laceration of
the Brachial Artery
-If the artery is completely occluded (or
severed), the resulting ischaemia can cause
necrosis of forearm muscles. Muscle fibres are
replaced by scar tissue and shorten considerably
– this can cause a characteristic flexion
deformity, called Volkmann’s ischaemic
contracture.
101.
102. DIET IN AKI
• Diet to be planned according ti phase of aki
• In oliguric phase –salt,potassium, fluids and proteins
are restricted and calories supplied mainly from
carbohydrates and fats
• In diuretic phase-fluid 300-500 ml more than urine
output. Sodium and potassium supplementation may
be required
103. • Calories-30kcal/kg body weight
• Proteins-0.5/0.6 g/kg(60% of high biological
value)
• Fluids-oliguric-urine output + 500ml,daily
weight loss of 0.2-0.3 kg in oliguric patient
104. • Sodium-signs of fluid overload, salt free diet,
diuretic phase salt intake liberalised
• Potassium-restriction in oliguric phase
105. DIET IN CKD
• Calories-30 kcal/day, 85% from
carbohydrates,10% from fats and 5% from
proteins
• Proteins-0.5-0.6g/kg/day(can be increased in
patient of dialysis)
• Sodium-if odema-upto 3g/day, if no
hypertension,odema-6 gm/day
106. • Calcium and phosphorus-dietary phosphate
binders calcium carbonate often prescribed
107. Diet in nephrotic syndrome
• Calories-30-40 kcal/kg
• Protein-1.5g/kg/day
• Fluid –if oedema restriction to equal to urine
output
• Salt-2-3 gm/day
