Crossing over and exon shuffling?
Crossing over primarily happens because of homologous recombination (HR). From the molecular point of view, it can happen between any homologous regions and it is not necessary that an entire allele has to be crossed over. During the process of HR, a DNA double strand break occurs. This is followed by resection (exonucleolytic degradation of one of the strands &mdash; 5'→3', from the break-point) by the MRX complex which leads to formation of ssDNA ends. The length of these ssDNA ends dictate the total length of crossover region. 


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   Taken from: Branzei, Dana, and Marco Foiani. "Regulation of DNA repair throughout the cell cycle." Nature reviews Molecular cell biology 9.4 (2008): 297-308.


This length can be from around 1.5kb to over 10kb depending on the repair kinetics with possibly an average of 3kb (more than half the cases) [1, 2]. Therefore, the author speculates that the probability of intra-gene crossover would increase with increase in intron length. However, in my knowledge, there are no recent reports to validate this hypothesis.

Edit:

Going back to the original question. It is not necessary that entire alleles are crossed over. Generally the genome has some recombination "hotspots" flanked by what are known as LD (linkage disequilibrium) blocks. An LD block need not cover an entire gene, as observed by Twells et al. (2003)[3] :


  LD breaks down in the region LRP5 g.5257T → G–LRP5 g.28149C → T, in
  intron 1 of theLRP5 gene. A second block of very strong LD
  (‖D'‖ > 0.9) is observed, LRP5 g.28149C → T–LRP5 g.45704G → A,
  spanning 17.6 kb of intron 1 to intron 3 of the LRP5 gene.




References:




Chung, Woo-Hyun, et al. "Defective resection at DNA double-strand breaks leads to de novo telomere formation and enhances gene targeting." PLoS Genet 6.5 (2010): e1000948.
Zhou, Yi, et al. "Quantitation of DNA double-strand break resection intermediates in human cells." Nucleic Acids Research (2013): gkt1309.
Twells, Rebecca CJ, et al. "Haplotype structure, LD blocks, and uneven recombination within the LRP5 gene." Genome Research 13.5 (2003): 845-855.