Left-side Ureteric Colic Case Study Essay

Case Study – Group B

Introduction

A 46 year old secretary was admitted to emergency with left-side ureteric colic. She had a similar case 3 years ago and she passed a small calculus spontaneously. She has been taking cimetidine (for the last 6 months), for dyspepsia treatment. Physical examination revealed a tenderness in the left loin.Left-side Ureteric Colic Case Study Essay

Symptoms

Left-side ureteric colic.

Small calculus passed spontaneously (3 years ago).

Tenderness in the left loin.

Medication Taken

Cimetidine (last 6 months) for dyspepsia treatment.

Serum Results (compared to ‘normal’)

Creatinine 150 umol/L (50-110)

Na+ 141mM (135-145)

K+ 4.2mM (3.5-5.1)

Total CO2 20nM (23-29)

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Urea 8.1Mm (4.0-8.2)

Albumin 40g/L (35-50)

Calcium 3.49mM (2.1-2.5)

Phosphate 0.60mM (1.0-1.5)

ALP Activity 160U/L (20-140)

Results that differ from ‘normal’ levels are underlined.

Suspected/Differential Diagnosis

This patient has been admitted to emergency with 3 major symptoms, all of which occurred within the last 3 years (symptoms are stated above). Along with this the patient has been subscribed cimetidine for the last 6 months which is advised to not be taken when the patient is known to have kidney problems, this could potentially be increasing the problematic symptoms.Left-side Ureteric Colic Case Study Essay

The most recent symptom, to which the patient was initially admitted, is left-side ureteric colic. This is caused by movement of the calculus that produces unpleasant sensations of abdominal pain often in waves (colicky) or sometimes a constant pain, both of which will typically move until it reaches the hypochondrium (or groin area). This supports the results from the physical examination which state that there was a tenderness in the patients left loin, due to the movement of the calculus and pain from there-forth.

These symptoms are most commonly developed after passing of a kidney stone, such as the small calculus that this patient passed 3 years ago. These stones can be static or moving, the latter of which can be more painful and cause more symptoms as it travels.Left-side Ureteric Colic Case Study Essay

Renal calculi are generally formed when the urine is overly saturated with minerals and salts such as calcium and others. This is supported by the patient’s blood-serum results which indicate a high amount of calcium (3.49mM) where the ideal level is around 2.1-2.5mM. Kidney stones are primarily made out of 60-80% calcium, so the excess amount found in the patient’s blood can easily result in a build-up of a calculus.

In addition to the excess of calcium, there is also an excess of other substrates in the blood. One of which is creatinine which is ideally found between 50-110 umol/L but the patient contains excess of 150 umol/L. High amounts of creatinine is known to effect the ability for the kidneys to filter fluid within the body. This will lead to a build-up of certain substrates in the blood such as the calcium mentioned previously. Therefore, high amounts of creatinine can cause a ‘domino effect’ where high amounts of creatinine = high amounts of other substrates, this could cause major problems in the body if not treated immediately.Left-side Ureteric Colic Case Study Essay

Also within the results of the patient’s blood-serum test is the abnormality of low amounts of CO2 (20nM) known as hypocapnia, this is can be used to indicate that the patient may be beginning to show signs of kidney failure.

Similarly, low amounts of phosphate are shown (0.60mM), this is also an indication of kidney failure due to inadequate filtration of substrates by the kidney to be excreted as urine. The parathyroid hormone (PTH) regulates the amount of phosphate and calcium in the blood, typically the substrates react oppositely: as phosphate increases, calcium will decrease. Due to there being a great excess in calcium the PTH hormone reacts to decrease the amount of phosphate in the blood serum.Left-side Ureteric Colic Case Study Essay

Finally, as phosphate is used to repair bones, help the function of nerves and muscle contraction, low amounts of it can cause a severe problem in the patient. This links into the high amounts of ALP activity that are found in this patient’s blood-serum at 160U/L which can be caused by stones such as the small calculus being obstructive. This can lead to problems with bones, which being linked to low amounts of phosphate also, could cause severe problems in the patient and even bone cancer. However, high amounts of ALP have been found in women in the third trimester of pregnancy, which could be the case with this patient, but this is currently unknown.Left-side Ureteric Colic Case Study Essay

Further Tests to confirm the diagnosis

Urine examination can be used to find if there is any blood in the patient’s urine (haematuria) which often occurs after passing a stone. Also the pH of the urine can be examined to indicate either the urine is ‘normal’, acidic (<6.0) which has the potential to result in a uric acid stone, or alkaline (>8.0) indicating that an infection could be present from organisms such as Proteus or Pseudomonas. As well as this, the urinalysis can show substrate crystals such as calcium oxalate- quite likely due to excess calcium in the patient.

Imaging (X-ray, Ultrasound etc.) Firstly, KUB x-rays can be used to show abnormalities in the kidneys, ureters or bladders, these are indicated by dark shadows in the renal-tract but can be mistaken for phleboliths which is venous and not a form of calculus.

Ultrasounds are easy and quick and does not use any form of radiation, this method will indicate stones that are of 0.5cm in diameter or larger.Left-side Ureteric Colic Case Study Essay

Next, Intravenous Pyelogram (IVP) provides a clear outline of the urinary tract system and shows-up many indicators of kidney problems such as mild hydronephrosis, however this test can cause unwanted reactions in the patient that are best avoided.

Finally, a test for the PTH hormone can be undertaken with the calcium, phosphate and ALP blood tests. This will help to identify hyperparathyroidism, which is a hyperactivity of the hormone, as well as finding the cause for the high amounts of calcium in this patient.Left-side Ureteric Colic Case Study Essay

Treatments and Prognosis

The patient that is suffering from left-side ureteric colic, small calculi and tenderness in the left loin should drink plenty of liquids, primarily water. This will encourage any further renal stones to be passed and it will also begin to reduce any possible damage to the functionality of urinary/renal tracts.Left-side Ureteric Colic Case Study Essay

If there are further stones found in the patient (possible due to high calcium amongst other substrate fluctuations) then with liquids they should pass spontaneously, unless they are large in-which they will need specific removal that could involve surgery. Spontaneous movement and passing of stones may take as long as 40 day so the patient is likely to be under a lot of pain that is often compared to being worse than child birth, therefore pain killers such as paracetamol at a standard dosage of 1 or 2 tablets up to 4 times a day for an adult such as this patient, may be required to alleviate the pain.

If by taking further tests, such as the urinary examination, it is found that the patient is suffering from an infection (pyonephrosis) then treatment is required such as percutaneous nephrostomy. This is usually an emergency procedure that is used to relieve an obstructed and infected renal collecting system by percutaneous puncture with ultrasound guidance.Left-side Ureteric Colic Case Study Essay

Also, Medical Expulsive Therapies can be used such as calcium antagonists. These work by blocking the calcium ion channels to supress the fast component for contracting the ureter, this in turn will help relax the smooth muscles and help stones to pass more easily.

Overall, the patient is likely to be in a lot of pain for some time, therefore, strong painkillers will be required and if in the case of infections then antibiotics could also be necessary to overcome the patient’s symptoms and to finally be cured.Left-side Ureteric Colic Case Study Essay

Case report
A 35-year-old man, with no previous history of
cardiovascular disease or abdominal trauma, was
examined by his family doctor because of an acute
pain in the left flank. On physical examination his
blood pressure was 130/80 mmHg on both arms and
the left costo-vertebral angle was tender. Urine
analysis revealed microscopic haematuria. Plain
abdominal radiography showed a single calcification
in the left lumbar area. On abdominal ultrasound,
neither renal stone nor hydronephrosis were seen
but the radiologist reported a dilated proximal left
ureter, suggesting a possible obstructive urolithiasis.
Surprisingly, the left kidney was smaller than the
right one (9.9 · 6.0 cm vs. 12.0 · 6.7 cm, respectively). In addition, intravenous pyelography (IVP)
showed absence of contrast in the left kidney after
50 min. Despite these abnormalities, no late IVP
images or blood analysis were made and the diagnosis of obstructive left ureteral stone was proposed.
Diclofenac and norfloxacin were prescribed and the
patient was discharged. Flank pain disappeared
within 24 h.Left-side Ureteric Colic Case Study Essay
Six weeks later, the patient presented intense,
pulsatile headache, accompanied by nausea and
vomiting and was admitted in the emergency
department at our hospital. Physical examination
revealed severe arterial hypertension of 210/
130 mmHg without papilloedema and/or focal neurological signs. Axillary temperature was 37.4 C.
Blood analysis showed an increase in serum creatinine (127 lmol L)1
), urea (9.1 mmol L)1
) and
total proteins (87 g L)1
). Total cholesterol was
5.7 mmol L)1
, HDL cholesterol 1.2 mmol L)1 (total
cholesterol/HDL cholesterol ratio: 4.7), and triglycerides 0.7 mmol L)1
. White cell count (9.0 G L)1
),
platelet count (336 G L)1
), haemoglobin
(160 g L)1
), calcaemia (2.4 mmol L)1
), serum albumin (48 g L)1
), creatine kinase (CK) (57 U L)1
),
aspartate amino-transferase (ASAT) (13 U L)1
),
alanine amino-transferase (ALAT) (12 U L)1
), and
C-reactive protein (CRP) (4 mg L)1
) were in the
normal range. Sodium (134 mmol L)1
), potassium
(2.9 mmol L)1
), and chloride (94 mmol L)1
) levels were
decreased. Urinary sediment and urinary catecholamines/metanephrines were within normal limits.
Renal ultrasound showed a further reduction of the
Journal of Internal Medicine 2003; 254: 605–608
2003 Blackwell Publishing Ltd 605
left kidney size when compared with previous
measurements (length of 8.1 cm vs. 9.9 cm).
Renal artery duplex images showed a dramatic
decrease of arterial blood flow in the main renal
arteries on the left kidney. Renal angiography was
subsequently performed, disclosing an aspect of
stump of the left trunk, subocclusion of the superior
arterial branch with multiple stenosis of secondary
branches and complete thrombosis of the inferior
branch (Fig. 1). The whole picture was compatible
with subtotal renal infarction and secondary renovascular hypertensive crisis. To our surprise, a
detailed analysis of renal arteriography revealed a
string-of-beads appearance of the superior arterial
branch, consistent with medial fibromuscular dysplasia (FMD). The right renal artery was normal.Left-side Ureteric Colic Case Study Essay
Thus, the hypothesis that FMD of the left renal
artery ultimately lead to arterial occlusion and
massive renal infarction was forwarded. In order to
assess the viability of left renal parenchyma, radionuclide imaging was performed. Residual left kidney
function was <5%, leaving to the right kidney most
of the renal function by compensation hypertrophy.
Unfortunately, the complexity of renal artery lesions
(multiple intra-renal arterial stenosis and thrombosis) together with the observation of a rapidly
progressing renal atrophy did not justify any
angioplasty, stenting procedures or surgical reconstruction.
Lisinopril 20 mg day)1 was prescribed and blood
pressure dramatically decreased. Cardiac echography excluded left ventricular hypertrophy and
there was no hypertensive retinopathy. At discharge, arterial pressure was 115/75 mmHg and
the biochemistry values were normalized. Angiotensin-converting enzyme (ACE) inhibitors were
maintained and, after 1-year follow-up, blood pressure, renal function and urinalysis were normal.
Discussion
The clinical presentation – acute flank pain and
microscopic haematuria in a young man – suggested an ureteral colic, rather than a massive renal
infarction. More than 90% of the patients presenting
with a renal infarction have a medical history
revealing a high risk of thromboembolism, i.e. atrial
fibrillation, previous embolism, valvular or ischaemic heart disease [1], which was not the case in our
patient. In addition, the initial absence of hypertension was misleading. Solez observed that hypertension was almost an universal finding in extensive
unilateral or bilateral renal infarctions [2].
The presence of haematuria in the setting of acute
flank pain is not very helpful indeed. Haematuria is
actually a poor predictor of ureterolithiasis. In a
recent report, 35% of patients with acute flank pain
associated with microscopic haematuria did not
have renal calculi [3].Left-side Ureteric Colic Case Study Essay Other diagnosis were urinary
infections, ureteral tumour, torsion of ovarian masses, appendicitis and diverticulitis. Renal infarcts
were not identified in that retrospective analysis of
195 patients, which confirms that this diagnosis is
probably rare. In our patient, the key finding was
the total absence of contrast after 50 min on IVP
associated with a reduced-size kidney. Such results
were not compatible with an obstructive lithiasis.
Thus, the absence of a typical clinical constellation
and the suboptimal interpretation of IVP and renal
ultrasound lead to a wrong diagnosis of ureteral
colic. As a matter of fact, the diagnosis of acute renal
infarction is often delayed or missed because of
unspecific clinical presentation and a relatively low
Fig. 1 Angiography of the left kidney: subocclusion, with stringof-beads appearance, of the superior arterial branch; complete
thrombosis of the inferior branch.
606 F. BARBEY et al.
2003 Blackwell Publishing Ltd Journal of Internal Medicine 254: 605–608
incidence [1]. Most patients presenting with acute
unilateral flank pain or abdominal pain are
recognized to have more common diseases, such as
urolithiasis, appendicitis, lumbago, or even myocardial infarction. Main laboratory abnormalities, such
as leucocytosis, elevated serum LDH and CK and
haematuria are common, nonspecific, and therefore
not helpful [1]. Slight elevation of serum creatinine
is frequently seen initially even if the renal infarct is
unilateral [4].
FMD is a small- and medium-sized arterial disease
that occurs more frequently in young Caucasian
women, leading to nonatheromatous and noninflammatory arterial stenosis; the right renal artery is
most often involved [5]. Histological subtypes include
medial (70–90% of cases), intimal, and periadventitial forms [6]. In our case, FMD affected a young
man, on the left side, and lead to renal infarction,
which is an exceptional event [7, 8]. Although
progression of FMD has been confirmed in a substantial number of patients with renovascular disease, Meaney et al. reported that in a long survey up
to 10 years, progression of lesions was observed in
only 16% of patients with FMD compared with 36%
of patients with atherosclerosis [9]. Other studies
demonstrated that progression of renovascular FMD
was seen in 36–38% of patients, without however
reaching complete occlusion of the vessel [10, 11].
Schreiber et al. followed 66 patients with medial FMD
for 45 months and found that none of them
progressed to complete arterial occlusion, although
some lesions became more stenotic [12]. In the series
of the Mayo Clinic, progression was more common in
intimal and peri-adventitial rather than in medial
FMD subtypes [13]. Furthermore, in contrast to
medial FMD, intimal and periadventitial subtypes
were sometimes associated with progressive dissection and thrombosis, resulting in renal arterial
occlusion [9]. The relatively slow progression of the
disease over time and the rarity of arterial occlusions
are unexplained. The cause of FMD is not known.
The disease is not seen in children and clinical
manifestations generally occur during the third and
fourth decade, mainly in Caucasian females. The
hormonal status is believed to play a pivotal role in
the development of FMD lesions. In this particular
case, the picture was compatible with an occlusion of
the main renal artery, as suggested by the observation of a total absence of contrast on IVP after
50 min. This event was likely to be secondary to a
superimposed thrombus on a previously narrowed
artery.Left-side Ureteric Colic Case Study Essay
The two-step course of hypertension in this patient
is quite instructive. The first ultrasound demonstrated that the left kidney was reduced. This observation
might suggest preceding parenchymal ischaemia.

However, the absence of ventricular hypertrophy
and of hypertensive retinopathy together with the
observation of an initially normal blood pressure
suggest that the patient did not have sustained
hypertension. Mechanisms responsible for sustained
renovascular hypertension differ upon whether one
or both kidneys are affected by vascular lesions,
either pathological or created in animal models using
clips. In the two-kidney one-clip Goldblatt model, the
presence of a normal controlateral kidney has
important consequences [14]. As the renin–angiotensin–aldosterone system is activated by the affected
kidney, the controlateral kidney is exposed to elevated arterial pressures and responds by excreting
sodium in far greater quantities than the stenotic
kidney. So, renin activity from the nonstenotic
kidney is suppressed to reduce arterial pressure.Left-side Ureteric Colic Case Study Essay
The record of a normal blood pressure in the
context of a massive renal infarction is another
intriguing observation. In animal models, complete
occlusion of the renal artery is usually associated
with the development of hypertension within hours
[14]. Irreversible renal parenchymal damage is
observed after only 3 h. In this patient, the main
renal artery occlusion induced a total flow stop for at
least hours, probably days. So, we hypothesize that,
without an effective parenchymal circulation, the
infarcted kidney might not have been capable of
releasing circulating vasoactive mediators. Six
weeks later, when the renal artery was partially
re-canalized, as demonstrated in Fig. 1, severe
hypertension was observed. The intense activation
of the renin–angiotensin–aldosterone system was
corroborated by the presence of hypokalaemia
associated with accelerated hypertension.
Prompt recognition of an acute renal artery
occlusion is mandatory since treatment, i.e. thrombolysis, embolectomy or percutaneous transluminal
renal angioplasty (PTRA), may minimize the loss of
renal function [15]. Development of collateral vessels is crucial since maintenance of tissue viability is
ensured, although perfusion is inadequate to produce urine [16]. This suggests that an attempt to
revascularize occluded vessels is warranted, despite
CASE REPORT: A YOUNG MAN WITH A RENAL COLIC 607
2003 Blackwell Publishing Ltd Journal of Internal Medicine 254: 605–608
several hours or days of complete occlusion. Angiography or MR angiography are the most
appropriate technique to show a delayed nephrogram through collateral circulation. In our patient,Left-side Ureteric Colic Case Study Essay
the rapid decrease of renal length (from 9.9 to
8.1 cm) during a 6-week period was compatible
with significant ischaemic degenerative lesions of
the renal parenchyma. In addition, angiography
revealed multiple intra-renal arterial stenosis and
thrombosis which rendered angioplasty or surgical
reconstruction totally hazardous and probably dangerous. With regard to hypertension, if interventional therapy is not indicated or impossible, ACE
inhibitors like in our case, or AT1 receptor antagonists should be the first choice antihypertensive
drugs provided the disease is unilateral.
In conclusion, this educational case suggests that,
in a young patient, the triad – acute flank pain,
microscopic haematuria and ipsilateral normal or
reduced kidney size on ultrasound – may suggest a
wrong diagnosis of urolithiasis. In the absence of
clear confirmation on initial investigations, angiography (or contrast-enhanced CT) should be performed to look for renal infarction and/or renal
artery abnormality. The initial absence of hypertension does not preclude the existence of FMD and/or
concomitant renal infarction. Left-side Ureteric Colic Case Study Essay