Sunday, November 29, 2009

Putty kidney

43 year old female came for USG evaluation of abdomen to rule out metastasis from carcinoma breast. This USG showing calcified mass in whole of the left kidney witch is maintaining the renal contour with posterior acoustic shadow suggestive of putty kidney.

Putty kidney is an end stage of infection with tuberculosis in the genitourinary tract, calcification may entirely outline a nonfunctional kidney.The radiologic appearance of this condition, completely calcified kidney which is associated with autonephrectomy, has been described as the putty kidney. It is very common to see the radiographic and CT appearance of putty kidney but unusual to see the USG features of putty kidney.

Saturday, November 28, 2009


One year old female baby came with history of persistent cough, difficulty in breathing and stridor. Baby also had weight loss and sometimes mild fever. Routine hematological investigations were normal. Chest radiograph and contrast enhanced CT scan showed below mentioned findings

Figure 1 a) Radiograph frontal view showing homogenous opacity lesion in the right upper and mid zone with broad base towards mediastinum. The lesion is causing shift of mediastinum and trachea to the contralateral side and compressing the trachea just above the carina (arrow head). The lesion is extending above the clavicle (cervico-thoracic sign) and erosion of posterior end of third and fourth ribs (Long arrow). C) Contrast enhanced CT scan axial section mediastinal window showing heterogeneously enhancing mass lesion in the right posterior mediastinum extending to middle mediastinum causing compression of the trachea. The lesion is showing multiple small foci of calcification (black arrows in fig c).


Primary mediastinal neuroblastoma accounts for 14% of all neuroblastomas. Common location is posterior mediastinum, where they arise from paravertebral sympathetic chain. Patient commonly present with chest pain, cough and respiratory distress due to airway obstruction. Chest radiograph is the initial radiological investigation to be done in such patients. It demonstrates homogenous opacity mass in the mediastinum. If the tumor is large, there may be extrinsic compression and displacement of trachea and main bronchus with mediastinal shift (fig a-c). Rib erosion and asymmetrical widening of inercostal spaces may be seen on radiograph. Intraspinal extension may be seen as loss of vertebral height with widening of neural foramina on lateral radiograph. Approximately 50% of the lesions show calcification on radiograph.

CT scan is usually done to confirm the presence of lesion, and it also helps to define the location and extent of lesion, adjacent organ involvement, or vascular involvement. CT demonstrates calcification in up to 90%. The lesion characterization has become better with the advent of multiplanar image reconstructions in MDCT. However MR imaging is the investigation of choice for better characterization and demonstration of full extent of mass, extradural intraspinal extension and chest wall invasion. The advantages of MR over CT are its direct multiplanar imaging and better contrast resolution, which can allow differentiation of vascular from non vascular lesions without the aid of intravenous contrast agent. MR is very often used to evaluate tumor involving spine and spinal canal.

Teaching point:

Radiograph is the initial investigation to be done in the mediastinal masses and one should be able to identify the lesion and arrive at differential diagnosis. CT scan and MRI are done to confirm the lesion, location, extent, adjacent organ involvement or vascular involvement and intraspinal extension.

Friday, November 20, 2009

Congenital CMV infection

CT scan of 5 month old male showing paucity of white matter, gross hydrocephalus with periventricular calcification and patchygyria suggestive of congenital TORCH infection most likely CMV infection.

Cytomegalovirus infection may be acquired prenatally or perinatally. Signs at birth, if present, are intrauterine growth restriction, prematurity, microcephaly, jaundice, petechiae, hepatosplenomegaly, periventricular calcifications, chorioretinitis, and pneumonitis. Later in infancy, signs are pneumonia, hepatosplenomegaly, hepatitis, thrombocytopenia, and atypical lymphocytosis. Diagnosis is by virus isolation or serology. Treatment is supportive. Parenteral ganciclovir can prevent hearing deterioration, but its use remains controversial.
Differential diagnosis: TORCH infection, Congenital lymphocytic choriomeningitis, Pseudo-TORCH syndrome, Tuberous sclerosis.
Pseudo-torch syndrome: A rare genetic syndrome characterized by a small head, eye disease and brain abnormalities.

Thursday, November 19, 2009

Medullary nephrocalcinosis

Ultrasonography of both kidneys in 9 year old female showing multiple areas of increased echogenicity involving all of the medullary pyramids consistent with nephrocalcinosis. The renal cortex is normal in echogenicity. There is no evidence of hydronephrosis.

Medullary nephrocalcinosis refers to calcification in the medullary pyramids rather than the renal collecting system. It is caused by a number of processes, but the three most common are : hyper-parathyroidism medullary , renal tubular acidosis and sponge kidney (tubular ectasia). Medullary nephrocalcinosis is usually associated with hypercalcuria and often with hypercalcemia. Primary hyperparathyroidism and distal renal tubular acidosis account for over 60% of these cases. The remaining 40% of cases are due to a variety of other causes of hypercalciuria, including milk-alkali syndrome, Cushing's syndrome, bony metastases, hyperthyroidism, hypothyroidism, sarcoidosis, furosemide therapy, and in this case, vitamin D therapy.
Ultrasonography is more sensitive than conventional radiography and CT and sonography is unusually sensitive in detecting this condition, and the sonographic changes predate any visible calcification and are generally more dramatic than the abnormalitie seen on CT. Nephrocalcinosis may affect some or ail of the pyramids. The deposits of calcium phosphate and calcium oxalate in the interstitium of the renal pyramids reverse the sonographic appearance of the normal kidneys. The pyramids are normally hypoechoic relative to the cortex. In its early stages it causes increased medullary echogenicity at the periphery of the pyramids and eventually involves the entire pyramids. With progressive calcification, shadowing begins. A regular arrangement of hyperechoic pyramids are seen which may shadow if large calcified foci are present, but not if the foci are numerous and tiny, as they are smaller than the beam width. Less frequently, calcification is seen in the renal cortex.

Cardiac hydatid cyst

CT scan of 58 year old male patient showing large well defined well capsulated hypodense lesion seen in the myocardium of the left ventricle with multiple daughter cysts within suggestive of hydatid cyst.
  • Hydatid disease is a parasitic infection caused by larvae of Echinococcus granulosus, which is still endemic in many sheepraising countries.
  • Hydatid cysts can be located in various tissues, although they are most common in the liver (50–70% of cases) and the lung (20–30% of cases) in humans.
  • Cardiac involvement in hydatid disease is uncommon, constituting only 0.5–2% of all cases of hydatidosis.
  • Heart involvement - LV – 60%, RV – 10%, pericardium – 7%, pulm Artery – 6%, left atrial appendage – 6%, and interventricular septum is rare – 4%.
  • Cardiac involvement occurs by invasion of the myocardium - Through coronary circulation or pulmonary vein from rupture of pulm cysts in to vein.
  • Signs and Symptoms •No symptoms due to its latency and slow growing nature unless it is situated in critical site. •Signs and symptoms are extremely variable and directly related to location and size of the cysts. •Precordial pain is the most common symptom and is most often vague and does not resemble angina pectoris. •Sudden rupture of intracardiac cysts is a frightful complication and can cause acute pericarditis or tamponade, acute pulmonary hypertension by embolization of several scolices, systemic arterial embolization, and severe anaphylactic shock can be life thretening.

  • Imaging - Echocardiography, CT, and MRI can show the cystic nature of the mass and its relation to the cardiac chambers •CT best shows wall calcification. •MRI depicts the exact anatomic location and nature of the internal and external structures and is the technique used for posttreatment follow-up.
  • The appearance of a hydatid cyst on MRI is usually a characteristic oval lesion that is hypointense on T1-weighted images and hyperintense on T2-weighted images. •A typical finding on T2-weighted images is a hypointense peripheral ring, which represents the pericyst (a dense fibrous capsule from the reactive host tissue). •A variety of tumors in the heart and a congenital pericardial cyst must be considered in the differential diagnosis; however, the multivesicular nature of the cystic mass and membrane detachment indicate the true diagnosis.
  • The cysts may be single or multiple, uni or multiloculated, and thin or thick walled. •More specific signs are •Cyst wall calcification. •Presence of daughter cysts and Membrane detachment.
  • •Surgery remains the treatment of choice in the management of hydatid disease. •Although antihelminthic drugs have been used in the preoperative and postoperative periods since 1977, extirpation of the lesion under cardiopulmonary bypass is recommended.
  • To conclude CT and MRI are helpful for localizing and defining the morphologic features of hydatid cysts. •Specific signs include calcification of the cyst wall, presence of daughter cysts, and membrane detachment. •CT best shows wall calcification, whereas MRI depicts the exact anatomic location and nature of the internal and external structures.

Wednesday, November 18, 2009

Antenatal diagnosis Chiary II malformation - Fetal MRI

Gravida two female with previous history of abortion came for fetal MRI to ruleout congenital malformation showing lumbosacral myelomeningocele (arrow in first and third image), tonsillar herniation and corpus callosum dysgenesis (arrow in second image). features suggestive of Chiary 2 malformation.

The Austrian pathologist Hans Chiari in the late 1800s described seemingly related anomalies of the hindbrain, the so called Chiari malformations I, II and III. Later, other investigators added a fourth (Chiari IV) malformation.
Types include
Type I - Is generally asymptomatic during childhood, but often manifests with headaches and cerebellar symptoms. Herniation of cerebellar tonsils
Type II - Usually associated with myelomeningocele leading to partial or complete paralysis below the spinal defect. Abnormal development of the cerebellar vermis andmedulla oblongata occur, and they both descend into the foramen magnum. Hydrocephalus is frequently present.
Type III - Type II associated with with an encephalocele.
Type IV - Lack of cerebellar development.

The Chiari II malformation is a complex congenital malformation of the brain, nearly always associated withmyelomeningocele. This condition includes downward displacement of the medulla, fourth ventricle, and cerebellum into the cervical spinal canal, as well as elongation of the pons and fourth ventricle, probably due to a relatively small posterior fossa.

Tuesday, November 17, 2009

MRI Brain in Carbon monoxide poisoning

18 year old boy came with dizziness, head ache, nausea and loss of conciousness. Gives history of overnight sleeping in the room with burning charcoal heater. MRI FLAIR and T2 (a&b) image showing bilateral symmetrical hyperintensities in globus pallidi. (c&d) diffusion weighted images showing no restriction. features consistent with carbon monoxide poisoning.

In carbon monoxide poisoning, the gas crosses the alveolar capillary membrane and binds strongly with heme containing compounds. The toxicity is due to hypoxia and carbon monoxide mediated damage at the cellular level. Globus pallidus and pars reticulata of substantia nigra are the regions of the highest iron content in the brain. Carbon monoxide directly binds to heme iron in these two regions.

MRI in acute carbon monoxide poisoning, the abnormalities are detected as T2 hyperintensities. Lesions are in the basal ganglia involving the globus pallidus, putaman, caudate nucleus with other areas such as periventricular white matter, subcortical white matter, cerebral cortex, medial temporal lobe (hippocampus) and cerebellum. Diffusion Weighted Imaging(DWI) and MR Sprectroscopy are also useful. Diffusion weighted imaging shows diffuse hyperintensity in periventricular white matter and semiovale, splenium of corpus callosum, internal capsules, and brainstem, with moderately decreased apparent duffusion co-efficient (ADC) values. In the globus pallidus, the ADC values are rather increased, with low signal intensities on DWI as seen in this case. The MRS (MR Spectroscopy) demonstrates decreases n-acetyl aspartase in bilateral basal ganglia.

Sunday, November 8, 2009

Focal Nodular Hyperplasia of Liver - CT and MRI

MRI of 30 year old female T1 weighted image showing well defined slightly hypointense lesion with central hypointense scar which is showing slightly hyperintense on T2 WI. In venous phase the lesion is showing homogeneous contrast enhancement (arrow). In delayed phase image there is enhancement of scar.

CT of another 28 year old female showing well defined showing arterial enhanging lesion in the left lobe of liver with central non enhancing scar. On venous phase image the lesion shows homogeneous contrast enhancement. In delayed phase image there is enhancement of scar.

FNH is considered a non-neoplastic, hyperplastic response to a congenital vascular malformation. Histologically, FNH is not a tumor and consists of benign-appearing hepatocytes occurring in a liver that is otherwise normal (i.e. no cirrhosis).
On CT scan the FNH are hypervascular lesions with homogeneous enhancement in arterial phase and hypodense central scars in arterial and venous phase, which enhance in the equilibrium phase. This is characteristic of FNH.
On MR typical FNH is slightly hypointense on T1WI and slightly hyperintense on T2WI. The scar is somewhat hyperintense on T2. The enhancement is as we expect with 'capillary blush' with a scar that enhances late in the equilibrium phase. We need to differentiate fibrolammellar carcinoma (FLC) of liver from FNH as the imaging findings are almost similar except for few differentiating points. The central scar is hyperintense on T2 in FNH where as it is Hypo in FLC. Scar enhances in delayed phase of contrast study in FNH where as it will not enhances in FLC. May see calcification in FLC and not in FNH.

Search This Blog